Neuro Sensory

Neuro-sensory
th
References: Neurology, a 4 year Student Teaching Resource by Drs David Abernethy and Stuart
Mossman, Wellington School of Medicine
See also Dementia and Delirium, page 439
Neurology ....................................................... 117

History ....................................................... 117
Physical Exam ........................................... 117
Cognitive Functions .................................. 122
Common Peripheral Nerve Lesions .......... 123
Brain Anatomy .......................................... 123
Intracranial Haemorrhage .......................... 123
Stroke ........................................................ 125
Head Trauma ............................................. 129
Coma and Stupor ....................................... 130
Syncope (Fainting) .................................... 131
Abnormal Speech ...................................... 131
Parkinsons Disease .................................. 131
Dystonias ................................................... 132
Demyelinating Disease .............................. 132
Other CNS Degenerative Diseases ............ 133
Epilepsy ..................................................... 133
Brain Tumours .......................................... 136
Spinal Chord Syndromes ........................... 138
Headaches ................................................. 139
Myasthenia Gravis .................................... 140
Other neurological emergencies ................ 140
Other.......................................................... 140
Eyes ................................................................ 140
History ....................................................... 140
Physical Examination ................................ 140
Anatomy .................................................... 141
Loss of Vision ........................................... 141
The Red Eye .............................................. 142
Glaucoma .................................................. 143
Eye Infections............................................ 144
Optic Nerve Lesions .................................. 145
Nerve Lesions Affecting Eye movement .. 145
Retinal Vascular Disease ........................... 145
Focal Ischaemic Retinal Disease ............... 145
Tumours .................................................... 146
Paediatric Ophthalmology ......................... 147
Vestibular ........................................................ 148
Ear ................................................................... 149
External Ear ............................................... 149
Middle Ear................................................. 149
Ear Testing ................................................ 150
Hearing Loss ............................................. 151
116 4th and 5th Year Notes

Neurology
UMN = Upper Motor Neuron, LMN = Lower Motor Neuron
History
Want to know the answer to two questions:
Where is the lesion (based on history and exam): Eg Weakness:
Upper motor neuron: motor cortex, internal capsule, brain stem or spinal chord
Lower motor neuron: nerve root, brachial/lumbosacral plexus, or peripheral nerve
Neuromuscular junction
Muscle
What is the lesion (based on history mode of onset and progression)? Is it infarct, haemorrhage,
inflammatory, tumour or degenerative
Differentials:
Inability to walk: Parkinsons, spinal chord (demyelination, compression, disease due to B12 or
syphilis), cervical spondylosis, polymyositis, myasthenia gravis, Guillain Barre, hereditary motor
and sensory neuropathy, MS, diabetic neuropathy, motor neuron disease, alcoholic neuropathy
Brief loss of consciousness: Stokes Adams attacks, VT, postural hypotension, hysterical
unconsciousness, vasovagal syncope (fainting), epilepsy, CVA
Coma and Stupor: hypoglycaemia, Wernickes encephalopathy, sedative or narcotic drug overdose,
post anoxic coma, CVA, status epilepticus, meningitis, encephalitis, delirium, coning. See Coma
and Stupor, page 130
Space occupying lesion: bleed, tumour, cyst, abscess, TB granuloma, AVMs, hydrocephalus
Physical Exam
Hard to incorporate with rest of physical exam do it on its own
Tailor the exam to the clinical problem (full exam can take an hour)
Avoid suggestion: rather than Is this sharp or do you smell the perfume say what do you feel/smell
Quick list:
Observe: including wasting and fasciliculations
Cranial nerves
Tone
Power
Reflexes
Coordination
Sensation: position, vibration, pin prick, light touch
Mental State Exam
Wanting to test:
Distributed cognitive function:
Attention/concentration
Memory
Word finding
Localised cognitive functions
Speech
Visuo-spatial
If suspicious from history need assessment of the following:
State of consciousness: alert, drowsy, stuporose, comatose (assess with GCS)
Other observations from mental state exam (See Mental State Examination, page 414)
Orientation: date, their name, age, who are their relatives
Remote or long-term memory: phone number, Prime Minister, recent events in the news
Registration and Immediate recall: Memorise 3 objects, recall after 3 minutes. Repeat 4 or 5 digits
in reverse
Others: abstract thinking, serial 7s
Can use Mini-mental status test: but not sensitive to subtle impairments
Language
If difficulty following instructions, appears confused, etc
Neuro-sensory 117
Requires assessment of spoken and written response to both spoken and written questions
Observations: fluency, word finding, grammatical errors, understanding questions
Naming objects: ask about whole object then parts wrist watch and strap
Repetition: No Ifs ands or buts
Auditory comprehension: Increasingly complex commands, eg Close your eyes, touch your left ear
with your right thumb and stick out your tongue
Writing: write a simple sentence, their name and address
Reading: read aloud
Cranial Nerve Exam
1: Olfactory: Smell. Not if doing general screen. Close eyes. Check each nostril patent then test (eg
scented soap on ward). Poor smell common (smoking, allergies, ageing). Also in Alzheimers,
Parkinsons, MS, chemotherapy. Most serious association: frontal lobe tumour, presents with
personality change, self-neglect, dementia
2: Ophthalmic nerve: lesions common and serious. Check if they normally wear glasses. Test:
Acuity: (use pinhole if theyve forgotten their glasses). Test each eye separately
Visual fields: confrontational testing: first just hold hands in each visual field and ask what they
see. Then wiggle one finger, then the other, then both, in all visual fields (or count fingers)
Red pinhead test: test for colour sensitivity more sensitive than acuity (good for vague
hemianopia). Loss of colour = desaturation. Blind spot = scotoma
Hemianopia:
Pituitary lesion bitemporal hemianopia (nasal retina affected). Bring red pin from affected
field into normal gain of red colour is convincing. Upper temporal field in one eye is
typically affected first
Parietal lesion visual inattention
3, 4, 6: Seeing double. Complicated to sort out
Look for ptosis
Smooth tracking: Fix on finger, draw H in the air, ask for report of diplopia, watch for one eye
lagging or nystagmus (a few beats in extreme gaze is normal)
Examine pupils at rest, light reflexes and near reflex
Voluntary eye movement:
Look up, down, left, right. Often elderly have trouble looking up anyway
Cover test: look at target, cover one eye, does other eye move? Reverse. Shows which is
fixing eye
If diplopia found, find field where its maximal. Weak eye moves less; good eye overshoots.
Use stick man drawn on tongue depressor
Problems locating target (overshoot and come back) ?cerebellar
5: Trigeminal Nerve
Sensory 5th: Test light touch and pinprick in all 3 divisions on both sides (separate pathways in the
brain stem). Test corneal reflex (early sign of lesion) patient looks up, use cotton wool on cornea
(more sensitive than sclera)
Motor 5th: jaw opening in midline (tests pterygoids). Jaw deviates to the side of weakness. Clench
jaw and palpate maesseters. Jaw jerk only if indicated
7: Facial Nerve. Wrinkle forehead and show your teeth (not smile). Look for lower face weakness.
Upper face (eg screw up eyes) better preserved in UMN, both similarly affected in LMN (eg Bells
palsy can be due to HSV, onset in days, recovery in weeks/months, rarely parotid tumour). Note
symmetry, fasciculation, and abnormal movements. Dont normally test taste
8: whispered voice at arms length, with patients eyes close. Mask opposite ear by rubbing your finger
and thumb together beside it.
9 (glossopharyngeal and vagus nerves): back of mouth, say ahh, uvula up in midline. Check
swallowing. Gag normally not tested if you do, test both sides. Unilateral absence abnormal,
bilateral absence may be normal.
11 (accessory): shake and shrug shoulders. Observe sternomastoid and trapezius at rest for wasting,
fasciculation, or dystonia. Look sideways, try to return head against resistance. Compare strength of
shoulder shrug on each side. Rarely useful, unless confirming site or suspected lesion. Always test
neck extension if diffuse muscle weakness if abnormal indicates lesion above C1/C2
12: Hypoglossal nerve. Tongue. Examine at rest then protrude. If fasciculation ?motor neuron
disease. Deviates towards the weak side. Push tongue into check against your finger. Try rapidly
alternating movements of protruded tongue or rapid la-la-la

INSERT Cranial Nerve Table
Neuro-sensory 119
Motor Examination
Observation for congenital maldevelopment, wasting, fasciculation and abnormal movements (tremor,
chorea, myoclonus, dystonia)
Assessment of tone: resistance to passive movement (must be relaxed). Tone due to:
Rigidity (Basal ganglia): uniform resistance to slow passive movement, may be jerky (cogwheel
rigidity). Affects flexors and extensors equally
Spasticity (upper motor neuron). Rapid passive movement maximal tone to start with,
decreases suddenly as muscle is lengthened. Most marked in flexors of arms and extensors in legs.
Due to reflex contraction to muscle stretch
Clonus: maintaining stretch (eg of ankle plantar flexors) further repetitive beating
Power: compare between sides
Test in position where patient has mechanical advantage: you shouldnt be able to win then if its
normal
Grade as follows:
0: no contraction
1: a flicker/trace of contraction
2: active movement with gravity eliminated
3: active movement against gravity but not against resistance
4: active movement against gravity and resistance, but reduced power (covers wide range
can classify as mild, moderate or severe weakness)
5: normal power
Motor exam of the arms:
Observe arms at rest, then outstretched with eyes closed (check for drift non-specific test). Look
for wasting of 1st dorsal interosseus and abductor pollicis brevis
Assess tone at elbow (flexion/extension and supination) and wrist (flexion/extension) with slow
and rapid movements
Arms (start at top and work down)
Shoulder abduction (deltoid, C5, axillary nerve). Arms out like chicken wings push it down
Elbow flexion (biceps, brachialis, C5-6, musculocutaneous nerve) pull me in
Elbow extension (triceps, C7, radial). Arm bent up in front - push me out
Wrist extension. (Extensor carpi ulnaris and radialis, C6-7, radial nerve). Extended cocked
wrist push it down
Finger extension (extensor digitorum, C7). Fingers straight out push them down just distal to
MP joint
Finger flexion (flexor digitorum, C8). Try to uncurl curled up fingers
Abduction of index finger (ulnar nerve, T1, dorsal interosseus)
Abduction of thumb (median nerve, T1, abductor pollicis). Try and push raised thumb down
into palm. Look for atrophy of thenar eminence
Motor Exam of the legs:
Observation of legs: while standing, walking, lying down. ALWAYS observe posture and gait:
movement of arms, stride length, broadness, smoothness. Stand with eyes closed and feet
together (Romberg test). Look for wasting of tibialis anterior and small muscles of feet
Check for tone
Check for clonus. Flex hip and knee to 45 degrees, externally rotate hip, rapidly dorsiflex foot and
hold. Two or three beats of clonus may be normal if symmetrical
Power in Legs (patient lying down):
Hip flexion (ilio-psoas, L1-2, lumbar plexus). Push down on raised straight leg
Hip extension (gluteus maximus, sciatic nerve, L5-S1). Lift ankle of straight leg
Knee Extension (quadriceps, femoral n, L3-4). Bend knee, try to push ankle in
Knee Flexion (hamstrings, sciatic nerve, L5 S1)
Ankle dorsiflexion (tibialis ant peroneal n, L4 5): push on top of foot while toes raised
Ankle plantarflexion (gastrocnemius, sciatic nerve, S1 2): push on bottom of foot
Ankle inversion (tibialis ant & Post, peroneal and tibial n, L4 5). Patient bends foot in and
try and pull it back
Ankle eversion (peronei, peroneal nerve, L5 S1): Patient bends foot out and try and pull it
back
Rapid leg tests:
If they can walk on their heals, then no foot drop (L5 or common peroneal)

If they can walk on their tiptoes, then no S1 lesion (plantar-flexion)
To test proximal leg function, crouch and stand up
Differentiating Upper and Lower Motor Neuron lesions
Upper Lower
Tone (unless acute), Spasticity or
Rigidity (mainly Parkinsons)
Wasting No Yes
Reflexes (unless acute)
Reflexes
Key is for them to be relaxed
Arm (Clench teeth if no response):
Biceps (C5/C6)
Triceps (C7)
Supinator (C5/C6)
Can also do finger reflex if suspect C8 lesion: tap your fingers while placed over outstretch fingers
of face up hand. Often normally absent
Leg (if no response, interlock fingers of both hands and pull just before tap)
Patella (hold knees up) (L3/L4)
Ankle (passively dorsiflex ankle) (S1). 3 ways: hand on dorsum of foot and tap hand, directly on
Achilles tendon, or kneel on chair with foot hanging off, tap Achilles tendon (most sensitive)
Grading reflexes:
0: absent
+-: just present
+: normal
++: brisk normal
+++: very brisk
Plantar responses: put patient at ease! Normal response is plantar flexion (down). If upper motor
neuron lesion, big toe up and other toes fan out (Babinski). Not positive if withdrawal response (hip
and knee flexion) due to over response
Superficial Abdominal reflexes: Not tested routinely. Stroke lightly with sharp object in each quadrant
towards midline. Normal reflex is contraction. Tires quickly
Co-ordination
Rapid alternating movements of hand: supinate and pronate hand rapidly (dysdiadokinesia)
Finger-nose-finger test. Not too fast (may mask intention tremour)
Heel-knee-shin test
Heel-toe walking: tests midline cerebellar vermis
Romberg: tests dorsal column sensory loss (ie proprioception). Rare in clinical practice
Important syndromes including ataxia:
Cerebellar haematoma: Sudden onset of progressive headache, vomiting, and inability to stand or
walk. Later progressive drowsiness, lateral gaze palsy from pontine compression. Decompressive
surgery can be lifesaving
Wernickes Encephalopathy: Confusion, ataxia, nystagmus. 6th nerve palsy. On recovery: impaired
short-term memory, confabulation. Common with prolonged vomiting, poor nutrition, not
confined to alcohol
Sensory test
Issue is where and why to test. What do you expect to find? Do this last so you have some idea what
to look for. Very easy to suggest to patient
Common scenarios:
Hemisensory loss: stroke, peripheral root and nerve lesion
Glove or stocking: spinal chord lesion or peripheral neuropathy
Get patient to close eyes. Stimulate at irregular intervals so patient cant anticipate them. Test from
abnormal to normal. Dont try to completely map just test key boundaries
Key Dermatomes:
Stand on S1
Sit on S3
Groin: L1
Neuro-sensory 121
Umbilicus: T10
Nipple: T5
T2 meets C4 on line connecting axilla: should be clear difference across this line in any lesion
between T2 and C4
Middle Finger: C7
Position sense: hold big toe by the sides, explain which way is up and down, then test. Has low yield in
practice. Try functional test: can they stand up with eyes closed?
Vibration: 128 Hz fork. On bony prominences (what do you feel?). Move up until its positive. Bunion
medial melleolus tibial tuberosity anterior iliac spine. Test fingers for completeness. First
sensation to go in progressive deterioration
Pinprick: Use large safety pin and discard after use. Toes, fingers, face (no more unless suspicious, eg
reflexes). Is it sharp or blunt? Can alternate sharp and blunt end to see if they can tell the difference.
More reliable than light touch if both damaged
Temperature: Not usually done if pin prick done
Light touch (cotton wool)
Others (not routine):
Two point discrimination
Stereognosis: recognising objects by their feel (coin, key, etc). Normal hand first
Graphaesthesia: write numbers on the hand
Sensory inattention: touch sides separately and together which is being touched?
Cognitive Functions
Localised Cognitive Functions
Dominant hemisphere:
Speech, reading and writing
Calculation
Praxis (higher motor control of learned movement)
Non-dominant hemisphere:
Neglect: visual, auditory, tactile
Dressing or constructional apraxia
Visuo-perceptual: object recognition (fragmented drawings) and faces (Prosopagnosia)
Prosody: Expressive aspects of speech
Attention/Concentration
Depends on the reticular activating system, thalamus, frontal and medial temporal lobes
Test: orientation in time and place, serial subtractions, spelling WORLD backwards etc
Memory
Implicit: learned responses, reflexes and motor skills
Explicit:
Episodic:
Left hippocampus: verbal, right visuo-spatial, faces, etc
Temporally specific personal experiences
Lost in diffuse brain disease (dementia) and bilateral limbic disease (amnesic syndrome)
Semantic:
Facts, concepts, words, meanings (eg object naming, what do you cut bread with, etc)
In the temporal neocortex (left)
Lost in dementia
Working memory:
Very short term recall: words, numbers, melodies
Under frontal lobe executive control: important for dual task performance
Patients can have damage to just one of working or long term memory (eg Korsakov)
Psychosis patients have normal working memory, but cannot make:
New memories (anteriograde): Word list learning
Retrieve long-term memories: recall public events, autobiographical details
Higher Cognitive Function/Executive Function
Situated in the pre-frontal area (non-motor frontal lobes)

Functioning best established from informants and observation
Clinical features of frontal lobe lesions:
Poor planning: cant initiate and carry out a sequence of actions to complete a goal, cant do two
things at once
Cant control impulses: irritable, irascible
Deterioration of personal relationships, social habits and hygiene
Dulling of curiosity and vitality, jocular, puerile
Lack energy
Common Peripheral Nerve Lesions
Patterns of presentations:
Unilateral defined areas of weakness/sensory loss in hand or foot
Peripheral neuropathy
Paraparesis: weakness of both legs. Rare but critical. Usually spinal chord lesion
Muscle disease (rare): initial proximal pattern of weakness neck flexion, shoulder abduction, hip
flexion
Hemiparesis due to stroke: 1/day in Wellington (this one is not peripheral)
Hand:
Common Lesions:
Ulnar neuropathy: Elbow compression weakness of finger but not thumb abduction.
Thumb adduction weak (paper test). Weakness of long flexors of 4 th and 5th fingers. Wasting
of interossei. Sensory loss on little finger
Median nerve compression in Carpal Tunnel Syndrome: weakness and wasting of abductor
pollicis brevis, with numbness of palmar surface of fingers 1,2,3 and lateral 4. Tingling/pain
which wakes at night
C7 Radiculopathy: pain from neck, shoulder, arm and forearm. Weakness of elbow, wrist
and finger extension
C6 Radiculopathy: Weakens elbow flexion and wrist extension. Sensory loss of dorsolateral
forearm, thumb and index finger
Radial nerve (Saturday night Palsy): Unable to dorsiflex the wrist or extend fingers or thumb.
Less Common Lesions:
Peripheral neuropathy: weakens small muscles of the hand, glove sensory loss
T1 root lesion: Weakness of small hand muscles, sensory loss on medial arm and often
Horners syndrome
Leg:
S1 Radiculopathy: Pain in back, buttock, thigh, leg, and foot, numbness of the lateral border of
the foot. Mild weakness of eversion and dorsiflexion, depressed ankle jerk
L5 Radiculopathy: Pain in back, buttock, thigh, leg, and foot, numbness of medial border of the
foot and big toe, weakness of inversion and dorsiflexion. No reflex change
Common peroneal nerve lesion from compression at the fibula head: Painless, severe
weakness of dorsiflexion and eversion, with normal inversion, and numbness on the lateral foot
and dorsum of the foot. Maybe sudden onset with severe footdrop. Ankle jerk normal. 80% of
nerve palsies causing foot drop recover over 3 4 months. Differentiating foot drop:
Common Peroneal Lesion L5 Lesion
Ankle jerk OK May be depressed (normally S1)
Inversion OK Weak
Eversion Weak
Brain Anatomy
Revise it!
Cerebro-spinal Fluid CSF:
Made in coroid plexus on floor of lateral ventricles and roof of 3 rd ventricle
Flow: Lateral ventricles foramen of Munro (intraventricular foramen) 3rd ventricle
Aqueduct of Sylvia 4th Ventricle via 3 foramen to cisternal spaces of subarachnoid space
arachnoid granulations venous sinuses
Intracranial Haemorrhage
Usually due to:
Trauma: typically extra/epi-dural or subdural
Neuro-sensory 123
Spontaneous (usually due to cerebrovascular disease): brain parenchyma and subarachnoid
Extradural Haemorrhage
Due to head trauma, especially with skull fracture (although not necessary in children)
Lentiform shaped arterial bleed ( high pressure rapid progression)
Skull fracture leads to one of:
Blood from middle meningeal artery forces its way between dura and inner table of skull (normally
intimately related) rapid, displacing cerebral tissue herniation
Laceration of dural venous sinus slow, delayed findings, less dense, less common
Dura fixed at sutures so doesnt go past these (eg will be bounded by coronal and lamdoid sutures)
Dura has two layers: the outer forming the internal periosteum of the calvarium, the inner forming the
septae which compartmentalise the calvarium
Subdural Haemorrhage
Following trauma: 50% also have a brain injury (swelling, contusion, laceration, etc)
Bleed from bridging vein into the space between the arachnoid and dura mater (low pressure slower
progression)
Risk in old people due to relative cerebral atrophy
Traverses right round the inside the calvarium: cresenteric shaped bleed, very flat (may need to look
carefully to distinguish from the skull)
Most common location is over the lateral aspects of the cerebral hemispheres
Poor prognosis due to large size and associated brain injury
Classification:
Acute < 3 days
Subacute 4 21 days
Chronic > 21 days (eg minor injury in elderly, hypodense (blood broken down), lots of midline
shift
If not detected, the haematoma undergoes organisation granulation tissue. This can rebleed
Subarachnoid Haemorrhage
Into the space between the dura mater and pia mater where CSF is
Bleed may be focal, or diffusely spread through subarachnoid space (will flow into sulci and be
bilaterally symmetrical)
Incidence: 15 per 100,000
Signs/symptoms: Sudden severe headache, loss of consciousness, meningism (neck stiffness, vomiting,
photophobia, fever), maybe focal neurological signs, fundi
Spontaneous: ruptured aneurysm (70%), Arteriovenous Malformation (AVM, 10%), hypertensive
bleed, bleed into a tumour, hypocoagulable state
Traumatic: injury to leptomeningeal vessels, rupture of intracerebral vessels, contusion, laceration
Aneurysm:
Mostly situated on the circle of Willis (ie 40% are at the junction of the anterior cerebral artery and
the anterior communicating artery)
Associated with connective tissue disorders (eg Marfans)
Mostly saccular rather than fusiform
Saccular: due to elastic laminar (?congenital) = Berry Aneurysm. No muscle layer and
thickened hyalinised intima
Fusiform: due to atheromatous degeneration
Mycotic: due to septic emboli usually more peripheral in brain
Dissecting: may extend either from aortic dissection or from internal carotid artery (complication
of angiography)
85% are in the anterior circle of Willis. Posterior communicating artery unilateral 3rd nerve
palsy (dilated pupil, ptosis, etc)
Arterio-venous Malformations:
Localised developmental failure shunt from an artery to a vein gradually dilates
distension of veins under arterial pressure
Most in the territory of the middle cerebral artery
Can present with haemorrhage or epilepsy
Investigations: CT, CSF if CT not helpful and no risk of ICP (make sure blood is not from a bloody
tap)

Treatment:
Analgesia, rest (maintain normotensive)
Rebleeding: 30% die from 1st bleed, 60% from rebleed (25% within 2 wks)
Clip or endovascular obliteration if GCS > 6
Vasospasm: 5 15% have stroke due to vasospasm (peak 3 10 days post bleed) despite all
treatment. Cause: ?oedema around vessels compression. Prevention with fluids, drugs and
monitoring electrolytes
Complications:
Acute: if intraventricular extension ependymitis obstruction of aqueduct acute obstructive
hydrocephalus. Also cerebral oedema and vasospasm of the affected artery ( infarct)
Delayed: fibroblast proliferation in arachnoid space and at granulations communicating
hydrocephalus
Hypertensive Intracerebral Haemorrhage
Mainly due to rupture of small penetrating vessels secondary to hypertension which causes:
Hyaline arteriolosclerosis in small arteries and arterioles weakening of vessel
Minute aneurysms
Main sites are: Putamen, thalamus, pons, cerebellum
Haematoma compression brownish discolouration of surrounding tissue
How old is blood on a film
On a CT:
< 24 hours: homogenous high density lesion, well defined margins, prognosis related to size of clot
Then oedema develops, increasing the mass effect, less homogenous
For the first week is hyperdense cf brain tissue (clotting contracting)
2 3 weeks isodense
3 4 weeks is hypodense cf brain tissue. Breakdown of haemoglobin osmotically active
particles water diffuses in.
On MRI:
T1: fluid is black: hypointense
T2: fluid is white: hyperintense
If contrast enhancement ring enhancement, then either an abscess or metastatic deposit
Stroke
= The acute onset of focal or global neurologic deficit presumably of vascular origin lasting > 24 hours
(WHO). This includes ischaemic stroke, intracerebral haemorrhage and subarachnoid haemorrhage
Aetiology:
Risk in NZ in 65 74 is 1:100, in 85+ is 1:30
80% due to atheroma, thrombosis and embolism, especially following heart (recent MI, AF, RF
disease) or vessel pathology
Nearly half the people having a new stroke are already in institutional care or needing help with
daily activities
25% of strokes are in people who have had a previous stroke
Differential to stroke: TIA, Migraine, Trauma, space occupying lesion (sub-dural haematoma, tumour,
abscess), infections, hypoglycaemia, delirium, MS and spinal chord pathology/injury
Isolated signs seldom due to a TIA or stroke: dizziness, unconsciousness
Site of Lesion
Site of lesion:
75% hemisphere
25% posterior circulation
20% lacunar
Pathophysiology: Brain has high and constant need for blood supply
Signs of cerebral involvement:
Dominant hemisphere: language disorder (dysphasia, middle cerebral artery)
Non-dominant hemisphere: disorders of knowing (agnosia) and doing (apraxia), visual or sensory
neglect
Loss of integrated cerebral function (eg cognitive impairment, memory, abstract thought)
Failure of inhibition of lower centres (eg spasticity and urinary incontinence)
Neuro-sensory 125
Seizure activity: abnormal electrical activity in brain tissue around areas of ischaemia
Hemianopia
Four classes:
Total anterior circulation infarction (TACI. Anterior = Carotid artery anterior and middle
cerebral arteries): language or visuospatial disorder (depending on side) + homonymous
hemianopia + motor deficit in two or more of face, arm or leg
Partial anterior circulation infarction (PACI): 2 of 3 of TACI criteria
Posterior circulation infarction (POCI. Posterior = Basilar artery posterior cerebral artery):
variety of presentations, including ipsilateral cranial nerve palsy with contralateral motor
and/or sensory deficit, isolated cerebellar dysfunction, isolated homonymous visual field
defect
Common lacunar syndromes (small deep white matter infarcts):
Pure motor hemiparesis
Pure sensory abnormality
Ataxic hemiparesis
Sensori-motor stroke
Dysarthria and clumsy hand
Signs of brain stem involvement:
Diplopia, bilateral weakness or numbness, vertigo, ataxia
Brain stem syndromes: *
Syndrome Structures Affected Symptoms
Medial Medullary due Hypoglossal nerve (12) Atrophy and paresis of tongue,
to Ant. Spinal or deviates to ipsilateral side
Vertebral artery Medial lemniscus Contralateral loss of discriminative
touch and proprioception
Pyramid Contralateral hemiparesis
Lateral Medullary, due Spinal trigeminal n. & tract Ipsilateral loss of pain/temperature
to Vertebral, PICA, on face
maybe AICA Spinothalamic tract Contralateral loss of
pain/temperature on body
N. ambiguous Loss of gag reflex, dysphagia,
dysarthria, swallowing problems
Inferior cerebellar peduncle Ipsilateral ataxia
Vestibular n. Nystagmus, vertigo
Dorsal motor n. Vomiting
Descending sympathetic Ipsilateral Horners syndrome
fibres
Basal Pontine Abducens Ipsilateral medial deviation of the

Syndrome, due to eye
Basilar and pontine Facial Ipsilateral paralysis of face
arteries Medial lemniscus Contralateral loss of discriminative
touch and position sense
Corticospinal tract Contralateral hemiparesis
Mediobasal Oculmotor Ipsilateral outward deviation of eye

mesencephalic Edinger-Westphal Ipsilateral dilated pupil, no light
syndrome due to reflex
aneurysm of posterior Corticospinal tract Contralateral hemiparesis
Circle of Willis or Red nucleus Contralateral cerebellar ataxia
Basilar
Transient Ischaemic Attacks (TIAs):

30% of untreated TIAs eventually have a stroke, aspirin reduces this by a quarter
Presence of carotid bruit not very sensitive for stenosis (ie can have stenosis without it, may not
have significant stenosis with it)
Surgery for carotid stenosis giving TIAs: beneficial if stenosis > 70%, risk of ipsilateral
stroke. Other studies less variable (NNT if asymptomatic = 17, if symptomatic then 6 7)
Angiogram morbidity = 1.5%, surgical morbidity 1.5 6.3% (if not vascular trained)

Also consider multi-infarct dementia
Management
Investigations:
FBC: exclude polycythaemia and anaemia. Do electrolytes and renal function
ESR: exclude vasculitis
Glucose
ECG/CXR for heart disease, AF
?CT 5% dont have a stroke, also exclude haemorrhage before antithrombotic treatment, and to
assess for carotid surgery (>70% stenosis)
Treatment:
Aspirin small improvement in outcome if not haemorrhagic
Heparin has a negative effect: although beneficial for DVT prophylaxis
Warfarin anticoagulation if mitral stenosis or AF
tPA if within 4 hours and there is visible evidence of infarct covering < 1/3 of MCA territory on
CT
Immediate anti-hypertensive therapy only if hypertensive encephalopathy is suspected (will have
papilloedema)
Assessment of swallowing by a speech-language therapist: 40% of hospitalised stroke patients
have swallowing problems, can aspiration. Gag reflex is not sufficient to indicate normal
swallowing. Nil by mouth until assessed (ie for 12 24 hours) unless clearly dehydrated
Watch for cerebral oedema over next 24 hours if large stroke. Restrict fluids, iv mannitol
Early rehabilitation: turning to prevent bed sores, limiting bed rest
Assessment for depression (common following stroke) and urinary incontinence
Prognosis
After 6 months, 1/3 are dead, 1/3 have moderate disability, 1/3 have good recovery
Poor prognosis if havent started to make a good recovery after 2 weeks (acute assessment not reliable)
Risk factors for poor prognosis: prior stroke, persistent incontinence, cognitive/perceptual deficits, poor
previous functional status or social supports, poor sitting balance
Vascular Pathology
Primary intra-cerebral haemorrhage:
Eg Sub-arachnoid haemorrhage or Intra-cerebral haemorrhage related to trauma
Due to high blood pressure or lobar haemorrhage (?due to amyloid deposition in vascular walls)
Ischaemic stroke:
Thrombotic: occlusion depending on collateral flow
Embolic stroke
Other: vasculitis, cerebral venous thrombosis, carotid artery dissection, etc
Extent of infarction depends on:
Adequacy of collateral flow (via circle of Willis). Little/no collateral flow for the deep penetrating
vessels supplying the thalamus, basal ganglia, and deep white matter
Presence of previous occlusive lesions
Location and rapidity of the occlusive process
Infarcts are of two types:
Haemorrhagic (red) infarcts
Non-haemorrhagic infarcts: pale, bland, anaemic
Thrombotic infarction
Arterial occlusion usually due to in-situ thrombosis over a plaque, or emboli
Most common sites for atherosclerotic involvement are:
Carotid bifurcation
Origin of the middle cerebral artery
Either end of the basilar artery
Neuro-sensory 127
Pathology Imaging
< 24 hours Cytotoxic intracellular oedema CT: normal. Subtle loss of grey-white matter
interface. Little/no mass effect
MRI more sensitive than CT in first 24 hours.
See cortical thickening and loss of sulci
MRI, T2: signal intensity
MRI, T1: signal intensity
1 7 days Tissue necrosis, maximal CT: hypodense, homogenous area with sharp
intracellular oedema, blurring of margins. Variable mass defect
grey-white interface, tiny MRI, T2: hyperintense
haemorrhagic infarcts
7 21 days Resolving oedema. Marginal CT: Isodense surpigenous bands and nodular
(Subacute) capillary ingrowth. Progressive regions develop in the hypodense infarct.
liquifications Infarcted white matter does not show density
change. Contrast ring enhancement
MRI: loss of previous hyperintensity.
Chronic Phagocytic removal of necrotic CT and MRI. Lesion becomes homogenous.
tissue. Cystic cavitation (esp in Approach density of CSF. Gliosis
white matter). Gliosis contraction. Dilation of adjacent ventricle.
(proliferation of fibrillary Overlying cortex is atrophic, enlarged sulci
astrocytes glial membrane) and cisterns. Stable by end of 3rd month.

Healing in the brain: dont want scarring as the remaining tissue doesnt need protection (its still
within the skull) and scar contraction would damage surrounding tracts. So instead of scarring,
you get gliosis and cavity formation
Embolic Infarction
Mural thrombosis emboli. Most common sources are plaques within the carotid arteries and cardiac
mural thrombi
Most commonly affects middle cerebral artery
Embolus responsible for ischaemia lyses within 1 5 days reperfusion into ischaemic brain (lost the
ability to autoregulate)
This leads to perfusion, especially of grey matter and basal ganglia (lots of capillaries). Oedema
(would be if thrombotic) mass effect. Cortical petechial haemorrhages. If these are extensive
and merge haemorrhagic infarct
CT: previously hypodense become iso/hyper dense
Haemorrhagic Infarcts
Usually secondary to embolic infarct
Result from high reperfusion pressure, or following anticoagulation in thrombotic infarcts (eg heparin)
May develop within 21 days following an embolic infarct
Difference between haemorrhagic infarct and Intracerebral haemorrhage:
Haemorrhagic infarct Intracerebral Haemorrhage

Inhomogeneous Homogeneous
Wedge-shaped or rectangular Round/Oval
Indistinct border Sharp margins
Predominantly cortical Predominantly white matter
Haemodynamic Infarcts
~ Border zone infarcts
Vaso-occlusive disease + disturbed autoregulation temporary uncompensated decrease in perfusion
pressure
Affects watersheds between vascular territories (may haemorrhagic infarct), especially between the
middle and anterior cerebral arteries
Can lead to transient ischaemic attacks and infarction
Lacunar Infarcts
Hypertension arteriolar sclerosis of the deep penetrating arteries of the:
Middle cerebral artery basal ganglia and internal capsule

Posterior cerebral and basilar communicating arteries mid-brain and thalamus
Arteriolar sclerosis hyaline disrupted lumen small infarct small round lacunae (hole)
Cerebral Venous Occlusion
Confined to certain patients: pregnancy, post-partum, diabetes mellitus
Head Trauma
Types of Injury
Effects of head trauma:
Direct trauma (eg under skill facture)
Cerebral contusion (local or contracoup)
Shearing: diffuse axonal injury petechial haemorrhage in midbrain, corpus callosum and
cerebrum
Cerebral swelling
Intracranial haemorrhage: epidural, subdural, subarachnoid, intracerebral
Concussion: no absolute definition but period of loss of consciousness and anteriograde or
retrograde amnesia
Types of skull fracture:
Simple: linear of vault
Depressed
Compound: open to skin or sinuses
Skull base rhinorrhoea or otorrhoea
Principal injuries from acceleration/deceleration injury:
Contusion: coup and coutracoup
Subdural haematoma from ruptured bridging veins
Diffuse axonal injury (shearing injury). Ranges from concussion (very mild, temporary,
physiological disturbance) to severe
Assessment
ABC
Gross assessment:
Localise injury by looking for lumps, depressed fractures, etc
CSF from nose or ears basal skull fracture
Neuro assessment:
Use level of consciousness: GCS best response to verbal, motor and eye response. See
Glasgow Coma Scale (GCS), page 481
Also pupillary size and exam, limbs
In diffuse injury the main enemy is ischaemia, which leads to oedema. In localised injury, oedema is
the main enemy acts like a mass lesion
Presume cervical spine injury until cleared:
Need 3 xray views: anterior, lateral and peg (open mouth to view facet joints of C1 and C2, and
odontoid peg)
Clearance requires clear X-rays AND normal exam. If x-rays clear but tender C spine then CT
Assess other systems
Investigations:
SXR for minor HI (OK now but were knocked out): mainly for medico legal cover!
Cervical spine Xray, even if minor, for occult dens or cervical fracture
CT brain if GCS < 15, neuro signs in limbs, cranial nerve palsy or CSF leak
Criteria for admission, etc:
Discharge if GCS 15, low velocity, no seizures or fractures, adequate supervision at home and
readmission checklist given to patient
Admit if: loss of consciousness/marked post traumatic amnesia or under 5 or over 50
CT indicated if GCS < 15 at 4 hours or < 9 at any time, seizures or focal neurological signs
Neurosurgical referral if compound head injury or GCS < 15
Raised Intracranial Hypertension (ICP)
Other causes of intracranial pressure:
Bleeding
Neuro-sensory 129
Neoplasm
Brain oedema results from:
Inflammatory lesions
Infarction
Head injury
Neoplasms
Types of brain oedema:
Vasogenic cerebral oedema: permeability of cerebral vessels
Cytotoxic cerebral oedema: rare. Toxic effect intracellular oedema
If severe acts as a space occupying lesions
ICP leads to displacement of CSF and compression of veins, then:
Herniation of the:
Cingulate gyrus under the falx
Parahippocampal gyrus past the free edge of the tentorium cerebelli
Cerebellar tonsils into the foramen magnum (fatal)
And pushing of the midbrain against the tentorium on the opposite side
Treatment of intracranial hypertension:
Aim: Keep ICP low. Principle danger is ICP ischaemia, transtentorial herniation (uncus of
temporal lobe on ipsilateral side) and coning
ABC:
Maintain airway. If breathing OK then lateral position. 100% O2
Intubate if GCS < 9
Aim to keep CPP (Coronary Perfusion Pressure) > 70. CPP = MAP less the greater of ICP or JVP.
Coronary blood flow = CPP / CVR (cerebral vascular resistance)
In general, keep BP normal:
If hypotension then perfusion pressure (bad)
Use colloids to maintain BP at 120 160 systolic (dont over-hydrate, especially infants)
Diuretic: frusemide 40 mg iv
Tilt head up venous return venous pressure perfusion pressure
O2 requirements by sedation (Propofol or barbiturates eg thiopentone) and cooling
Hyperventilate reduce CO2 to 30 35 mmHg cerebral blood flow cerebral blood
volume brain volume ICP (but only for short term otherwise ischaemia)
Cushing's Reflex (bradycardia, hypertension) kicks in when O2 falls below 20 mls/100g/min
Mannitol 0.5 1g/kg over 20 mins iv if life threatening draws fluid from brain, but also a
diuretic, so watch for hypotension
Drain fluid from ventricle if severe
Evacuation of intra-cerebral bleeds
Seizures: Clonazepam 0.25 mg/min up to 1 mg plus loading dose of phenytoin
Nutrition, urine and bowel management
Steroids not effective after head injury
Coma and Stupor
Checking eyes:
Dolls Eye: do eyes remain fixed on target when head is turned. Tests inputs from the neck
muscles. Requires linking via medial longitudinal fasiculus of nerves 3, 4, and 6 on both sides
Vestibulo-Ocular reflexes: caloric response. 1 ml of ice water evokes nystagmus beating to the
opposite side in a normal person. If unconscious, see only deviation without corrective nystagmus
In deepening diffuse coma without structural damage, the Dolls eye disappears, then the Caloric
response. If pupils still reactive then no coning
Due to Structural damage
Only if affecting brain areas required to maintain consciousness: usually infarct, bleed or inflammation
Reticular Activating System: periventricular grey matter from mid pons up, including the hypothalamus
and deep grey matter of both hemispheres
Most supra-tentorial lesions produce coma due to oedema compression of deep hemispheric
structures (paramedian diencephalon)
Features of coning:
Transtentorial: progressive drowsiness followed by pupil changes

If unilateral cerebral swelling then stretching of ipsilateral 3 rd nerve parasympathetic
innervation
If diffuse bilateral swelling involving brain stem then impairment of both sympathetic and
parasympathetic mid position, irregular pupils
Posterior fossa coning: headache, stiff neck, BP, pulse
Due to Diffuse depression of brain function
Usually metabolic encephalopathy
Key differential from structural damage: Pupillary reflexes retained
Features: clouded consciousness, difficulty concentrating, altered sleep wake patterns
Two basic types:
Delirium or acute toxic psychosis: agitated, hallucinatory, severely disorientated
Acute confusional state: quieter than delirium
Immediate evaluation: Glucose, thiamine, Na, Ca, Creatinine, pH, PO2, PCO2, lumbar puncture, sepsis
(septicaemia, lung, urinary tract, meningitis)
Later: LFT, Sedatives, Blood and CSF culture, Electrolytes and Mg, Coagulation, EEG (absence status)
Outcome:
Sedative drug poisoning: equivalent to GA and will recover with treatment
Other medical causes: depends on cause, severity and extent. Only 15% make a good recovery if
in coma for more than a few hours
Traumatic: better outlook, related to age, 50% die (many instantly), if ophthalmologic signs of
brain stem dysfunction then 90% die or remain vegetative
Syncope (Fainting)
Temporary loss of consciousness (ie up to a minute or so)
In physically or emotionally stressful situations (eg sight of blood), going out with new partner or boss
Vasodilation from alcohol, warmth or drugs may contribute
Usually standing or sitting
Often groggy and unwell afterwards
Myoclonus common (seizure like movements, vocalisations): only 10% motionless
Due to cerebral blood flow:
Postural Hypotension
Cardiac output: arrhythmia, VT, periods of asystole (Stokes Adam disease)
NOT due to: TIA, hypoglycaemia, alcohol. These take longer to recover
Abnormal Speech
Types:
Dysphonia/dysarthria: problems with the mechanics, not ideas, of speech production (eg nerves
involved in motor control, connective tissue disease, etc). Say baby hippopotamus
Brocas (expressive) dysphagia: Non-fluent speech with malformed words. Reading and writing
are impaired but comprehension intact. Patients understand questions. Inferio-lateral frontal
lesion
Wernickes (receptive) dysphasia: Empty fluent speech. Maybe mistaken for psychotic speech.
Reading writing and comprehension are impaired. Posterior Superior temporal lobe lesion.
Cerebellar disease: ataxia of the muscles of speech slurred and irregular speech
Pseudo-bulbar palsy: UMN. Exaggerated jaw jerk, difficultly swallowing, maybe emotional
liability. Due to upper motor neuron lesion above the mid pons due to bilateral CV disease, severe
MS or motor neuron disease
Bulbar palsy: LMN eg facial nerve, Guillian Barre, etc
Assessment:
If speech fluent, grammatical and meaningful or patient can repeat a sentence dysphagia
unlikely
If the patient can comprehend simple instructions with several steps Wernickes unlikely
Parkinsons Disease
Bradykinesia, tremour (70% of cases) and rigidity (unilateral onset) but no early difficulty with gait
Also lack of arm swing (usually only one side at outset), lack of facial expression, paucity of
movement. 30% become demented (either due to Alzheimers or widespread Lewy bodies). Also
postural hypotension
Neuro-sensory 131
Gradual progression and prolonged course
Pathology:
Gross: Pallor of substantia nigra
Micro: in melanin-containing dopaminergic neurones with secondary reactive gliosis. Lewy
Bodies may be present in remaining neurones (eosinophilic intracytoplasmic inclusions).
Treatment:
L-Dopa dyskinesias, and on-off effects after 3 5 years. The mainstay of treatment. Give
minimum dose to control symptoms, not necessarily signs
Carbidopa: prevents peripheral conversion of L=Dopa
For younger patients, begin with a dopamine agonist (bromocriptine, pergolide)
Selegiline, a MAOB inhibitor delays the time needed for the subsequent introduction of L-Dopa
Anticholinergics: stop ACh induced hyper-reactivity: but dry mouth, urinary retention, blurred
vision
Other causes of Parkinsonism. Parkinson Disease is a disease of exclusion:
Drug induced parkinsonism eg phenothiazines including antiemetics (eg Maxolon)
Multisystem atrophy: also have cerebellar ataxia, eye movement disorder, autonomic dysfunction
and pyramidal signs
Huntingtons Disease: early presentation may mimic Parkinsons, rather than a movement disorder
with chorea, myoclonus and dystonia
Wilsons Disease: consider in younger patients. Behaviour disturbance, dystonia, flapping
tremour. Rare but treatable
Diffuse Lewy Body Dementia: Males 2:1. All demented eventually. Most have rigidity,
bradykinesia but tremour uncommon. Usually begins with cognitive impairment. See Dementia,
page 439
Dystonias
Most dystonias are caused by basal ganglia disturbance
Blephrospasm
Causes eyes to close all the time, especially in light, wind, etc
Tx: inject botulinum toxin
Hemifacial spasm
Cervical dystonia: neck turning, head back, etc
Demyelinating Disease
= Selective, primary destruction of myelin
Diseases of CNS and PNS myelin do not affect the other
CNS Demyelinating disease:
Multiple Sclerosis
Acute Disseminated Encephalomyelitis
Progressive Multifocal Leucoencephalopathy (PML)
Toxins
Leucodystrophies
PNS Demyelinating Diseases:
Guillain-Barre Syndrome
Diphtheria
Diabetes Mellitus
IgM Paraproteinaemia
Leucodystrophies
Hypertrophic neuropathies (eg Charcot-Marie Tooth Disease)
Secondary Demyelination:
Infarction
Abscess
Contusion/Compression
Multiple Sclerosis
Chronic autoimmune demyelination of CNS neurons
Epidemiology:
Female to male = 2: 1
Peak age of onset 20 to 40 years

Marked racial difference in susceptibility. Caucasian most common. Africans/Asians rare
Genetic risk modified by environmental risks up to age 15 (from studies of immigrants)
Risk 15 times higher if first degree relative with MS. Associated with HLA-DR2 haplotype
Can be sensory or motor
Diagnosis: Two lesions in different places at different times. Lesions normally visible on MRI
One spinal chord lesion may account for diffuse symptoms. As it grows through a spinal chord column
a single lesion may progressively affect other areas
Highly variable course. Relapsing and remitting
Worse after exercise
Pathology:
Autoimmune destruction of oligodendrocytes, ?triggered by a viral infection in a genetically
susceptible host
Multiple plaques distributed throughout the cerebral hemispheres (especially periventricular white
matter), optic fibres, brain stem, cerebellum and spinal chord
Active plaques: are soft yellow or pink and granular. Myelin breakdown foamy macrophages,
T-suppressor cytotoxic cells, T-helper cells, and plasma cell infiltrate. Also reactive astrocytes
Chronic plaques: well defined, sclerotic and grey. Sharply defined areas of demyelination with
compacted astrocytes processes ( gliosis)
Lesions expand by concentric outward growth. Poor correlation between number of plaques and
symptoms
Tx: -interferons
Progressive Multifocal Leukoencephalopathy (PML)
Like MS: multiple discrete foci of myelin destruction with relative preservation of axons
Caused by JC virus (DNA papovavirus common in the community) in immunodeficient patients
Relentlessly progressive
Pathology: multiple lipid laden macrophages, oligodendrocytes with ground-glass nuclei (viral
inclusions)
Other CNS Degenerative Diseases
Amyotrophic Lateral Sclerosis (ALS)
Most common form for progressive Motor Neurone Disease
Affects upper motor neurones (ie layer five of the motor cortex) and lower motor neurones (anterior
horn cells)
1 3 per 100,000 per year
5 10% autosomal dominant, rest sporadic
Cause unknown
Clinical presentation:
Lower motor neurons: fasciculations, progressive wasting of muscles, bulbar involvement
difficulty chewing etc, weakness of respiratory muscles
Upper motor neurons: spasticity, muscle stiffness, hyperreflexia
Sensory, bowel, bladder, ocular movements and cognitive functions relatively preserved
Median survival 3 years
Pathology:
Neurons shrink and accumulate lipofuscin
No macrophage or inflammatory response
Disappearance of axons in Corticospinal and corticobulbar tracts astrogliosis lateral sclerosis
Epilepsy
See Seizures, page 625 for Epilepsy in Childhood, Benign Febrile Convulsions and Anoxic Seizures
1:200
Onset after age 20 10% chance of tumour
Symptoms:
Abrupt onset, brief duration, rapid recovery, and stereotypical recurrence
Not just fits: focal signs depending on where in the brain it arises
Very long list of differentials to epileptic seizure: See Other Spells, page 136
Neuro-sensory 133
Is it epileptiform:
Pseudo-seizure (or Non-Epileptic Seizure): either factitious disorder (are deliberately faking) or
conversion disorder (they think its real) (See Somatoform Disorders, page 439)
Hard to differentiate: going blue, frothing at mouth and incontinence can happen in pseudo-seizure.
Epiletics may not have post-ictal phase
Gold standard is EEG: but cant do this in A&E. Fall back is checking whether the person is in
any way aware (then it cant be generalised) eg localising to pain (sternal rub, squeeze thumb
nail), drop their hand onto their face
Check history: evidence of brain injury, infection, on anticonvulsant meds
Pseudo seizure more common in women (10:1) and those with a medical connection (eg
doctor/nurse in family, someone with epilepsy)
Epileptic seizures happen more if: tired, ill, fever, stressed, not taking medication (but these are not
classified as provoked as they wouldnt provoke a seizure in a normal person)
Seizure Types
Generalised: bilaterally symmetrical without local onset
Tonic-clonic (Grand mal) seizures: Tonic phase: 10 20 secs extension phase then tremour
begins repetitive relaxation of tonic contraction. Clonic phase: usually 30 seconds, random
movements, tongue often bitten
Absence (Petit Mal) Seizures: Characteristic type of absence attack. Childhood or adolescent
onset, associated with 3/sec spike and wave on the EEG. Blank stare and unresponsive for 5 15
seconds. No post-ictal confusion or sleepiness. May also have automatisms and mild clonic
motion (usually eyelids at 3 Hz). May be induced by hyperventilation. 80% have no further
seizures after 20 years old. Can also have atypical absence seizures. Treat with ethosuximide or
sodium valproate
Atonic: complete, sudden loss of tone completely collapse, may injure themselves
Tonic: sustained contraction, maybe with fine tremour
Myoclonic: Sudden, very brief jerk but still generalised
Clonic: rhythmic jerking
Infantile spasms:
Sudden bilateral symmetrical jerk, extensor or flexor. Can be subtle, come in clusters
Usually around 3 6 months, boys > girls
Grow out of the spasms
Bad prognosis: cerebral palsy, retardation, etc
Medical emergency: try to urgently get them under control
Partial: Begin locally
In simple partial seizures consciousness is preserved.
Complex partial seizures are focal seizures in which consciousness is altered (eg blank
unresponsiveness followed by automatisms, eg lip smacking, other semipurposeful activity)
usually temporal lobe but may be frontal. Can go on for minutes. Aware it is coming (cf absence
which is sudden)
Partial seizure secondarily generalised: they have an awareness first
Localising it:
Preceding aura: olfactory, visceral, auditory, visual, dj vu
Dystonic posturing: contraction of agonist and antagonist muscles
Post-ictal Todds Syndrome: if they have one area of weakness after a seizures (ie one hand
weaker than the other) then it started locally
Automatic behaviour usually seen in complex partial seizures: but can be in absence (petit mal)
seizures. Eg Oral or manual automatisms
Seizure location:
Frontal: focal tonic or clonic motor activity, posturing, prominent motor automatisms but no
orofacial or experiential automatisms
Central: focal clonic seizures with preservation of awareness
Temporal: experiential, gustatory or olfactory hallucination. Motion arrest, automatisms
Parietal: exclusively somatosensory manifestations
Posterior: polymodal sensory, visual, auditory or somatosensory hallucinations
Sorting out type of seizure:
When do the seizures occur
Does patient know theyre going to have a seizure

What can the patient recall
Detailed description from observers:
Are they aware will they respond
Are their automatisms
Is there dystonic posturing
How long did it last
After the seizure: are they confused, can they speak, any post-ictal Todds
Treatment
Diagnosis is clinical. EEG helps with severity, classification, to localise a surgically remediable
abnormality (eg hippocampal sclerosis), and to differentiate pseudo-seizures
Dont treat until youre sure its epilepsy
Anticonvulsants suppress seizure activity in 80%
Principles of drug treatment:
When to treat: often wait for second seizure although treatment after the first occurrence, but
no long term change in outcome
Use only one drug
Tailor drug to seizure type
Introduce slowly. Takes about 5 days to stabilise a change in dose
Monitor drug level: for other than phenytoin, this is to check compliance. Beware plasma level
at which seizure control is obtained is variable
Consider withdrawal of drugs after 2 years without seizure, slowly over 6 months
Mode of action unknown but may GABA breakdown, as well as modifying flux of Na, K and Ca
ions
Usual drugs:
Idiots guide: carbamazepine for partial seizures and Valproate for generalised
Seizure type Examples of conventional drugs
Partial Seizures Simple partial, Carbamazepine (Tegretol),
Complex partial and Phenytoin, Sodium Valproate
Partial secondarily generalised (Epilim), Penobarbitone,
Primidone
Generalised seizures Absence Clonazepam (a BZD),
Ethosuximide, Valproate
Myoclonic Valproate
Tonic-clonic Carbamazepine, Phenytoin,
Valproate, Penobarbitone,
Primidone
Conventional drugs have hepatic clearance

Side Effects:
General lethargy, concentration, unsteadiness, dizziness
LFTs: but serious hepatotoxicity rare. Especially Valproate
Rarely bone marrow suppression
Pregnancy:
Epilepsy often worsens during pregnancy
Plasma concentration of drugs falls due to pharmokinetic changes and compliance
Teratogenic: 3% risk of malformation on 1 drug (also, epilepsy itself can be teratogenic -
?hypoxia during seizure)
% in breast milk varies by drug
Specific drugs:
Carbamazepine: enzyme inducer
Phenytoin: Dose-dependent kinetics small in dose may in plasma concentration,
SE: ataxia, peripheral neuropathy, gingivitis
Must be seizure free (with or without treatment) for 12 months before you can drive. Obliged to tell
LTSA on diagnosis if the patient wont and continues to drive
Status Epilepticus
Repeated seizures without regaining consciousness
No one knows how long is too long: but after 10 minutes risk of damage
Neuro-sensory 135
If not sure whether its epileptiform then must still treat for status
Treatment:
Protect and maintain airway, insert oral airway
Prevent injury
100% oxygen
Diazepam 10 20 mgs iv, not exceeding 2 5 mgs per minute. If no iv access give rectally with
10 20 ml normal saline. Duration is brief and another anticonvulsant is required. Avoid
repeating diazepam cardiorespiratory collapse. If no response give clonazepam 1 4 mg iv
Phenytoin 50 mg/min iv (25 mg/min in cardiovascular disease), usual adult dose 1250 mg in 100
mls saline over no more than 20 minutes. Monitor BP and heart rate
If established, give phenobarbitone
If refractory, then anaesthesia with propofol or thiopentone. Taper after 12 24 hours
Other Spells
Commonly misdiagnosed as seizures
Paroxysmal non-epileptic events without altered consciousness: Jitteriness, migraine with focal aura,
hyperventilation, acute paroxysmal vertigo, shuddering attacks, anxiety states (eg panic attack),
psychosis, drug induced dystonias, masturbation, tics, etc
Paroxysmal non-epileptic events with altered consciousness: Day dreaming, breath holding spells,
reflex syncope, TIAs, psychosis, pseudo-seizures, delirium, metabolic disorders, other brain insult
(infection, haemorrhage), ritualistic movements, migraine, arrhythmias, drugs substance abuse
Paroxysmal non-epileptic events related to sleep: benign sleep myoclonus of infancy, head banging,
night terrors, hypnogogic jerks, sleep walking, sleep apnoea
Brain Tumours
Epidemiology
2% of all cancer deaths
20% of paediatric neoplasms (21 per 100,000 at 2 years)
Incidence 8 10 per 100,000 per year
Incidence lowest in teens rises to 16 per 100,000 in 70s
Histology
Cell types in the brain: neurons, microglia (lymphocytic derived, phagocytic function), oligodenrocyte
(myelination), choroid cells (make CSF), astrocytes (structural support, star shaped, multiply in sites of
injury), ependymal cells (line ventricles), meninges, pituitary, lipophages (histiocytes which
phagocytose lipid rich myelin non-specific marker of white matter destruction)
Neuropil = intercellular matrix in the CNS tangled processes of neurones, astrocytes,
oligodendrocytes
Tumour vasogenic oedema
Incidence of neoplasms:
Neuroepithelial (ie intrinsic brain cells) Gliomas: 52%
Astrocytoma: 44%. When severe = Glial Blastoma Multiforme (GBM)
Ependymoma 3%
Oligodendrioglioma: 2%
Medulloblastoma: 3%
Metastatic 15% (eg breast, lung)
Meningioma: 15%
Pituitary: 8%
Vestibular Scwhannoma: 8%
Also retinoblastoma
Different incidence in children:
Normally posterior fossa (as opposed to anterior fossa in adults) and different frequencies of
different types
Most common tumours are pilocytic astrocytoma and medulloblastoma
Astrocytoma
Locally invasive

Presentation:
ICP from obstructive hydrocephalus and from space occupying lesion
Focal neurological deficit
Epilepsy: of high grade astrocytoma present with seizure
Endocrine
By age:
Cerebral hemispheres in middle and old age
Spinal cord in young adults
Cerebellum and pons in childhood
Pathology:
Benign = wont recur if removed. However, also need to be accessible to have a good prognosis
Heterogeneous range from well-differentiated to anaplastic
Characteristic fibrillary background of cytoplasmic processes containing Glial Fibrillary Acidic
Protein (GFAP). Can use immunohistochemistry to stain for these. May congregate to form
Rosenthal fibres
Graded from 1 (low grade, and hard to differentiate from reactive gliosis although these rarely
produce a distinct mass) to 3 (anaplastic) to 4 (glioblastoma multiforme GBM, mitoses common
compared with low grade, pallisading necrosis differentiates it from grade 3). Low grade have a
tendency to become high grade and are also hard to cure due to their infiltrative nature
Grossly: Infiltrative. Either firm or soft/gelatinous. GBM is heterogeneous with focal
haemorrhage and necrosis
Pilocytic variant of astrocytoma: most common astrocytoma of childhood. Excellent prognosis.
Cystic. Usually in cerebellum
Astrocytomas (grade 3 or 4) are the most common gliomas to arise subsequent to radiotherapy
(usually 5 25 years later)
Investigations: CT and MRI. Xray and angiography obsolete
Management:
Dexamethasone: vasogenic oedema ICP
Anticonvulscents seizures
MR spectroscopy biopsy by framed stereotactic or image guidance
Surgery: debulking or macroscopic excision (only if not deep or eloquent areas otherwise too much
damage from surgery use radiotherapy for these)
Arguments for macroscopic excision. High-grade gliomas weigh 100g at diagnosis = 10E11 cells.
After macroscopic excision will still have 10E10 cells. Effective radiotherapy 10E8 cells.
Chemo/radio therapy only kills cells in division
Prognosis
For GBM: Median survival:
Without surgery, 17 wks
With surgery, radio and chemo, 51 wks
For low grade glioma: 50% 5 year survival if total macro excision
Other Neuroepithelial Tumours
Subendymal giant cell astrocytoma: associated with tuberous sclerosis
Neuronal tumours: not common. Include:
Gangliocytomas
Gangligliomas: better prognosis
Cerebral neuroblastoma: Rare, in children. Resemble peripheral neuroblastomas small round
blue-cell tumours
Oligodendroglioma:
5 15% of gliomas
Radiographically, well demarcated and often show calcification (key differential)
Grossly: gelatinous masses +/- cysts and/or haemorrhage
Ependymoma: usually in fourth ventricle outflow obstruction. Also in intramedullary portions of
the spinal chord. Slow growing and not malignant but poor prognosis. CSF spread is common.
Significant histological features: true rosette and perivascular pseudo-rosette. Numerous subtypes
Choroid Plexus Papilloma: rare. In ventricles. Usually children. Cauliflower type projections into
ventricular lumen
Neuro-sensory 137
Pineal Neoplasma: Intrinsic tumours are Pineocytoma and Pineoblastoma. Germ cell tumours are the
most common, including choriocarcinoma, teratoma, etc. Present with mass effects in men aged 20
40. Differential: lymphoma or metastatic cancer
Hemangioblastoma: Highly vascularised, cystic tumours, mainly in the cerebellar hemispheres
Craniopharyngioma: Arise from the epithelium of Rathkes pouch part of the embryonic nasopharynx
the forms the anterior lobe of the pituitary. Present due to mass effects in children and adolescents.
Histology: see keratin pearls.
Primitive Neuroectodermal Tumours (PNETS):
Rare tumours in children arising from primitive glial or neuronal precursor cells. Aggressive and
poor prognosis. Usually small round blue-cell tumour (differential includes lymphoma)
Medulloblastoma: a distinctive PNET. Occurs exclusively in the cerebellum, mainly in children,
mainly as a midline mass. Cause CSF obstruction and spread via CSF
Scwhannoma: In the cranial vault, nearly all schwannomas are attached to the 8 th cranial nerve in the
cerebellar pontine angle acoustic neuroma
Lymphoma: Either originated in the CNS or from systemic invasion (usually affect the meninges).
Usually B-cell lymphomas
Pituitary
Pituitary Adenoma: benign neoplasm in anterior lobe of the pituitary
Present with either mass effects (including on the rest of the pituitary) and excess hormone
secretion
At any age or sex, but most common in men aged 20 50
Classified on the basis of hormones they secrete by immunocytochemistry. Poor correlation
between acidophils, basophils and chromophobes and the hormones secreted
Carcinomas are rare. Diagnosis requires gross brain invasion or discontinuous spread
Metastatic Brain Tumours
20% have intracranial mets at autopsy
In 15% primary organ not found
Surgery for solitary met if primary site controlled or for symptomatic control or for diagnosis
Most mets are carcinomas. 80% are due to (in decreasing frequency): lung, breast, skin (melanoma),
kidney and GI
Prognosis:
Melanoma & lung solitary: < 30% 1 year survival
Breast solitary: 50%
Undetermined solitary: 50%
Meningioma
20% of primary intracranial neoplasms
Incidence peaks in females aged 40 - 50
Benign in 90 95%
Occur anywhere round brain
Well circumscribed mass effects
Histology: meningothelial whorls and psammoma bodies
Tx: surgical excision
Spinal Chord Syndromes
Prognosis depends on time to treatment: speed is important
Trauma:
Transfer to specialist unit within 24 hours unless medically unstable
Catheterise: bladder wont work urinary retention
Check underneath them before transferring. An unfelt pen or other object will cause a full
thickness pressure sore during 2 hour transfer 3 months to heal
200 per year in NZ (same as severe HI). Mainly young men long term disability, lots of
ongoing psychological problems
Extradural spinal cord compression (EDSCC)
Usually cancer. Also haemorrhage (epidural haematoma) or epidural abscess
Key questions: where is the lesion, what is the lesion (eg weight loss, past cancer history
cancer)

If there is a clear level below which these is sensory abnormality spinal chord
If both legs then spinal chord (usually). Can be parasagital meningioma (very rare)
Are arms normal: if so T2 highest possible level
If there are signs of an upper motor neuron lesion in the legs then it MUST be above the cell
bodies of L3 S5 in the conus of the spinal chord, which is at T12 vertebral level if UMN
lesion then it is in thoracic spine or above
95% have pain at the site of compression very good indicator. Tap gently down spinal chord
with tendon hammer
Imaging: MRI
If cant be completely sure its cancer MUST biopsy (eg chronic infection)
Cancers:
Lymphoma
Female: breast
Male: lung, sometimes prostate
Transverse Myelitis:
Inflammation of spinal chord itself
Same symptoms as EDSCC, but no compressing signs on MRI (usually normal NO mass lesion)
Usually due to a demyelinating type inflammation can be due to MS (= 2 demyelinating lesions
in the CNS at different times and different places)
Could also be sarcoidosis granulomas and inflammation (very rare to only occur in spinal
chord)
Corda Equina Syndrome (CES)
Triad: leg weakness, sensory loss, sphincter problems (usually overflow not urgency ie LMN)
Classic description: saddle anaesthesia anaesthesia in sacral dermatomes eg feels like cotton
wool when sitting on the toilet seat. May be only symptom. Usually bilateral
If due to central disc prolapse can be fixed if treated urgently medical emergency
95% of disc prolapses are at L4/L5 or L5/S1: but most are laterally into nerve root, not central into
cauda equina
Acute Inflammatory Demyelinating Polyradiculopathy (AIDP)
= Guillian-Barre
= Demyelination of multiple peripheral nerves
Symptoms: ascending paralysis. Affects arms, legs and respiratory. Only a portion will get to
ventilatory arrest, but can deteriorate very quickly test FEV1 4 hourly while normal (normal >
4 l), to ICU if < 2 l. (O2 saturation and PO2 wont tell you till too late)
Predominantly motor problem: unlikely to be AIDP if lots of sensory symptoms
Signs: LMN and arreflexia (arreflexia is a classic sign)
Tests:
Lumbar puncture: protein but no WBC
Nerve conduction studies: motor conduction < 30 m/sec (normal > 40 50 m/sec)
Treatment: IV globulin and plasmaphoresis (plasma exchange). Heparin to prevent PE
Not related to Chronic Inflammatory Demyelinating Polyradiculopathy
Headaches
See also Headaches, page 624 for Headaches in Children
Recent onset of severe headache: the most common cause is idiopathic
Ask about associations/antecedents
Red flags: fever, change in mental status/personality, fits, focal neurological signs, sudden and severe,
affected by postural change, normally headache free, waking at night or in the morning with a headache
Types of headache:
Tension headaches, eg chronic daily headache, gradual onset (chronic), sleep not disturbed, treat
by stress (massage, relaxation). ? Depression. Types: post-coital, ergotamine misuse
Cluster headache: clusters of extreme, recurrent non-throbbing deep pain in and around an eye,
spreading onto the face. Eye typically becomes swollen and watery
Migraine: visual symptoms, unilateral, throbbing, nausea, aura
Facial structure: eg TMJ dysfunction, sinusitis, NOT teeth
Neuralgic: eg idiopathic, trigeminal neuralgia
True vascular headache: associated with TIA/stroke, artery dissection, giant cell arteritis
Associated with ICP: focal lesions, venous thrombosis, meningitis, severe hypertension
Neuro-sensory 139
Acute: ?meningitis, sinusitis, head injury
Associated with post Lumbar puncture
Treatment: Ongoing unchanged tension or migraine headache: TCAs
Differential of morning headache:
ICP
CO2 (eg sleep apnoea)
Diabetic going hypoglycaemic overnight
Myasthenia Gravis
Antibodies to Ach receptors weakness, fatigues with repetition
Affects eye movement in 15%
Treatment:
Immunosuppressives: Prednisone, azathioprine, cyclosporin
Take out thymus many have hyperplasia or thymoma
Myasthenia Gravis Crisis:
Triggers: Respiratory infection, change in medication
Respiratory failure due to weakness, can be insidious
Consider ICU admission and ventilation
Other neurological emergencies
Meningococcal meningitis. See Infections of the CNS, page 495.
Encephalitis: fever, stiff neck, strange behaviour, unable to make new memories, seizures. Acyclovir
10 mg/kg 8 hourly (> 20% caused by Herpes Simplex)
Temporal arteritis/Giant Cell Arteritis: See Giant Cell arteritis/Temporal Arteritis, page 282
Other
Trigeminal neuralgia: momentary severe shooting pain in one division of 5 th nerve due to touching,
chewing or speaking. Responds to Tegretol
Locked-in syndrome: pontine infarction quadriplegia and variable loss of all reflex and horizontal
eye movements. Vertical eye movement or eyelid movement may be the only means of
communication
Cerebellar infarction/haemorrhage: vertigo, headache, and abnormalities of eye movements (eg
saccadic deficits). May lead to life threatening compression/coning of the brainstem
Eyes
History
Common presenting complaints:
Loss of vision: blurred, double, distorted, field loss, glare, colour defect
Disturbance of sensation: pain, itching, photophobia. If sharp pain surface, if throbbing pain
deeper lesion
Changes in appearance: red and/or discharge
Associated symptoms
Past ocular history: trauma, surgery, spectacles
General medical history: diabetes, allergy, medications
Family History: squint, glaucoma, refractive error
Social History: Assess impact on function (eg work, hobbies, support, dependents). Also smoking
incidence of cataract
Physical Examination
Trying to work out where is the problem: refractive, obstruction of light through the transparent tissues
of the eye, or neural problem
Measure Visual Acuity:
One at a time. Wear glasses
Snellens Chart: Distance of chart (normally 6 metres)/Distance they could read. Smaller fraction
is worse
If cant see chart at all, then Count Fingers (CF) at X metres
If cant count fingers then Perceive Light (PL): flash torch on and off in eyes can they see it

Check with pinhole, if clearer refractive error or corneal scarring, refer to optometrist. If worse
retinal pathology
Also check visual fields, colour, stereo vision
External inspection:
Be systematic: look for changes in shape, size, position, colour, transparency, is it focal or diffuse
Pupil reflexes: Should be simultaneous and equal. Swinging light test: Alternate light from one
eye to the other, swapping it quickly. Both pupils should stay the same. Sensitive and complete
test of neural pathways. If this shows a problem, test for an efferent pupillary defect with the near
reflex test
Internal inspection with ophthalmoscope:
Get patient to look at target a long way away: relaxes accommodation. Dim the light dilation
Dilate pupil with Madriasil (not atropine, T too long)
Check for:
Red reflex defects: eg cataract, intra-ocular blood
Reduced transparency (compare two eyes)
Cup and disk:
Disk is 15 degrees nasal to fixation. To examine macula, get patient to look directly at the
light
Check disk for distinct margins and symmetry
Physiology cup is blood vessels in the centre of the nerve not nerves
Normal cup to disc ratio < 1/3 (but lots of variation). Check its the same in both eyes
Large and/or deep cup sign of glaucoma (vessels diving into the cup) especially if eyes
different. Large ratio
Papilloedema: non-inflammatory nerve oedema due optic nerve axon flow obstruction or ICP
red disk swelling towards you, blurred margins of disk but no early visual loss. Venous
obstruction may haemorrhage. If bilateral then ICP
Papillitis: optic nerve head inflammation swollen disk with visual loss. If unilateral then
optic neuritis (colour vision, orbital pain), sarcoidosis, Tb, Syphilis, etc
Pseudopapilloedema: occurs in hypermetropia, disc is smaller than normal and crowded
Fundus pathology: maculopathy, optic neuropathy, retinal detachment
Refractive errors: hard to focus on retina
Arteries: narrow, bright red, windy. Veins: thicker, straight
Amount of melanin in choroid layer variation in pigmentation of retina. Deep green patch =
coronial nevus (benign)
Clinical usefulness depends on good instrument, good technique, knowledge of normal anatomy
and normal variations
Anatomy
Fovea: dip in middle of retina. Only photoreceptors, neural connections heaped up around it
Macula: ill defined area around fovea
Uvea = iris, ciliary body and choroid. Iritis = anterior uveitis
Reflex pathway: retina optic nerve optic chiasm optic tract lateral geniculate nuclei
optic radiation and brain stem Edinger Westphal nucleus 3rd nerve
Loss of Vision
Is it bilateral or unilateral?
Sudden: Woke up with it Vascular: Central retinal artery or vein occlusion, ischaemic optic
neuropathy, vitreous haemorrhage, CVA, preretinal haemorrhage
Suddenish: Gradual over a few days: Closed angle glaucoma (hours), infection, inflammation, retinal
detachment, optic neuritis
Gradual: Months to Years: Refractive, cataract, primary open angle glaucoma, age related macular
degeneration, retinopathy (eg diabetes, hypertension)
Chronic visual loss:
Uniocular Binocular
Cornea & Red Reflex Keratoconus, cataract, uveitis Corneal dystrophies, cataract,
uveitis
Visual Fields Retinal detachment, meningioma Retinitis pigmentosa, pituitary
lesions
Pupils and IOP Glaucoma Glaucoma
Neuro-sensory 141
Dilate for Fundoscopy Malignant melanoma, optic Maculopathies, optic atrophy,
atrophy papilloedema
Age Related Macular Degeneration
Loss of visual acuity with peripheral vision in tact
Observe stippling and depigmentation of macular
Can be uni or bilateral
Age-related types:
Dry (atrophic) macular degeneration: thinning of macula, gradual. No cure. Atrophy of
photoreceptors, loss of outer nuclear layer
Wet (exudative) macular degeneration: May be due to Choroidal Neovascular Membranes,
unilateral with onset over several weeks. Straight lines appear wavy refer as laser treatment
slows progression
Symptoms: blurred central vision, distortion of straight lines
Eye Trauma
Mechanical: blunt/sharp, superficial/penetrating
Chemical: alkali the worst. Local anaesthetic then irrigate for 30 minutes (less time already irrigated
before presentation). If not toxic nor significantly inflamed, if VA OK and no fluorescein staining then
chloramphenicol eyedrops qid for 5 days
Radiation: UV, thermal, arch flash. Comes on hours after exposure, is very painful. Eye is very red,
multiple fine specks of fluorescein staining. Usually resolves in 24 hours. Treat as an abrasion (pad
both eyes)
Hyphema: blood in anterior chamber. Refer for opinion but dont normally treat. Check for corneal
abrasion, traumatic mydriasis, eye movements, blowout fracture of orbital floor, intra-ocular bleed
Penetrating Eye Injuries can be missed by subconjunctival bleed. Always refer if at risk. If metal vs.
metal, always do an xray otherwise blind from Fe toxicity. Also rose thorns. Teardrop shaped cornea
is a PEI until proven otherwise. Refer immediately. Lie down, im antiemetic to prevent vomiting.
Keep nil-by-mouth
Distorted pupil: penetrating injury until proven otherwise nil by mouth, shield eye, antibiotics,
antiemetic, refer
Foreign bodies: remove with 25-gauge needle and topical anaesthetic drops. Steady fixation of eye is
key. Always evert upper key lid to look for further foreign bodies
Corneal abrasions: Very painful and photophobic. Stain with fluorescein. Most heal within 24 hours.
Refer if abrasion large or central, if cornea hazy, VA reduced or eye is very inflamed. Double pad eye
well. Apply chloramphenicol ointment stat and bd for 5 days. Never give anaesthetic drops to take
home can cause ulceration and blindness
Lid laceration: sow up anything not penetrating, or not involving lid margin or tear drainage (refer
these)
Retinal Detachment
Higher risk in near-sighted (myopic)
Can be caused by blunt trauma
Due to vitreous shrinkage, tears/holes in retina (eg with age), or underlying pathology
Symptoms: sudden changes in vision watery or shadowy patch, sudden in number of floaters (spots
in vision), loss of visual field (like a descending curtain)
Need rapid treatment: seal tear with laser
Causes:
Exudative detachment: accumulation of fluid under the retina due to leaky vessels, eg tumour,
vascular abnormality
Traction detachment: vitreous becomes organised following trauma or neovascularisation and pulls
on the retina
The Red Eye
Never use steroids in an undiagnosed red eye (can worsen ulcers, etc)
Diagnostic Tree:
Uniocular:
No Pain, vision normal: subconjunctival haemorrhage, episcleritis, pterygium, conjunctivitis
Pain and normal vision: if no corneal staining: Anterior uveitis, scleritis, HZO. If corneal
scarring: HSV, marginal ulcer

Pain and vision reduced: If no corneal staining: severe uveitis, angle closure glaucoma,
secondary glaucoma. If corneal staining: HSV, Bacterial keratitis, HZO
Binocular:
No pain, good vision: bacterial, viral or allergic conjunctivitis
Pain, vision good or poor: viral or chlamydial keratoconjunctivitis
Subconjunctival bleed: self limiting unless severely hypertensive or coagulopathy
Conjunctivitis:
Initially unilateral, may bilateral due to cross infection
Feeling of surface grittiness
Causes:
Infective: See Eye Infections, page 144
Allergic: eg eczema, allergy to protein deposits on poorly cleaned soft contacts
Chemical/mechanical
Baby: 1 month with pussy discharge urgent referral (?blocked and infected lacrimal duct)
Never pad a discharging eye
Blepheritis
= Lid inflammation
Eyelash dandruff
Meibomian gland dysfunction: usually staph infection. 30ish glands under they eyelid normally
secrete lipid to cover tear film
Clean with saline or bicarbonate solution
Chalazion: Red nodule in the lid. Due to obstruction and infection of a Meibomian gland.
Microscopically granulomatous inflammation (basically a burst sebaceous gland)
Corneal Ulcer: See HSV infections below.
Keratitis:
Corneal inflammatory disease
Symptoms: deeper, aching pain
Aetiology: infective, contact lens, staph hypersensitivity, exposure keratopathy (eg 7 th nerve palsy)
Signs: speckled light reflex corneal oedema
Shingles affecting face: refer within 7 10 days to check for intra-ocular complications. Pain is due to
trigeminal neuralgia
Iritis:
Frontal headache, photophobia, not watering. Usually unilateral
White cells and fibrous exudate in anterior aqueous. May be white cells at bottom of cornea
Usually autoimmune: Ankylosing Spondylitis, Crohns. Treat with steroids, and dilating drops to
keep iris mobile
Rarely infective (eg Tb)
Episcleritis:
= Localised inflammation of sclera. Treatment: topical NSAIDs
Acute onset, mild pain, young adults, usually sectorial, no corneal signs
Cf Scleritis: pain, VA decreased, tender, sectorial or diffuse, corneal signs
Pterygium:
Conjunctival overgrowth growing over cornea. Age related changes due to sun exposure
Refer if enlarging and vascularised. Differential: squamous cell carcinoma.
Pinguecula: White epibulbar nodule similar to pterygium
Acute Glaucoma: See Primary Closed-angle Glaucoma, page 144
Glaucoma
Usually due to outflow obstruction: damage to the trabecular meshwork overlying the channel of
schlemm resistance to flow steady state intraocular pressure vascular perfusion of the
neural tissue blindness
Classification:
Primary:
Open angle (chronic)
Closed angle (acute)
Secondary: eg iritis, trauma, blood in the eye, etc
Neuro-sensory 143
Primary Open-angle Glaucoma
Epidemiology:
Leading cause of preventable blindness
Risk factors: age, near-sightedness, African/Asian ancestry, family history, past eye injury, a
history of severe anaemia or shock, steroid medication
Most common sort, gradual impairment of aqueous drainage, insidious loss of sight
2% of over 50 years
1 in 7 risk if primary relative has it
Presentation:
Central field defect arcurate shape with macular sparing
Cupping of the disk due to ischaemic atrophy of the nerve fibre layer
Bullous keratopathy oedema of the cornea
Screen with tonometry (measuring intra-ocular pressure), test visual fields.
Is diagnosed by cupping of the optic disk: not by intra-ocular pressure. 17% of people with glaucoma
have normal IOP.
Pathology:
Resistance to outflow (pathogenesis not clearly understood) aqueous humour intra-
ocular pressure (normal is < 22 mmHg)
Leads to damage to ganglion nerve cell axon (final output) at the optic nerve head. Due to vascular
insufficiency as nerves exit the eye
Affects peripheral bundles preferentially: spares papillo-macular bundle
Treatment: Medication, laser treatment to enlarge the drain (trabeculoplasty)
Primary Closed-angle Glaucoma
Iris is pushed forward and acutely occludes the trabecular meshwork drainage
Rare but vision threatening
Unilateral, acute visual loss, pain, nausea and vomiting, dilated, non-reactive pupil
Precipitating factors: long sited (narrow anterior chamber, narrow iridocorneal angle), and when pupil
dilated for a long time (dim light)
Can be congenital
Once resolved, put hole through iris (iridotomy): no further obstruction possible
Secondary Glaucoma
Secondary open angle glaucoma: Outflow system is obstructed mechanically by debris (ie gunge up
trabecular meshwork). Rare. Eg Haemolytic glaucoma, lens protein glaucoma
Secondary closed angle glaucoma: Can be due to neovascularisation zipping up the angle, secondary
to ischaemic eyes (eg diabetes, central retinal vein occlusion)
Eye Infections
Viral Infections:
Adenovirus types 8 (epidemic) and 3 and 7 (sporadic). Conjunctivitis with pre-auricular lymph
node hyperplasia. Over about a week get small white spots (WBC accumulations) just below the
surface of the cornea
HSV:
Gives Herpes Simplex Keratitis.
Dendritic ulceration with neovascularisation. Chronic inflammation and scarring. May lead
to small white vesicles around the eye.
Viewed with fluorescein drops under cobalt light (stains where there is no epithelium)
Branching pattern Herpes Simplex Virus. Never give steroids: worse infection
permanent damage
Bacterial: Usually puss. Always bilateral:
Standard bacterial conjunctivitis: treatment chloremphenicol eye drops
Trachoma: Due to Chlamydia. Commonest cause of blindness in the tropics. Less common than
other causes in NZ. Chronic. Suspect if no response to topical antibiotics. Initially the
conjunctival epithelium is infected scarring of the eye lid abrasion of cornea over years
get panus (fibrovascular layer) over the cornea
Gonorrhoea: pre-auricular nodes

Optic Nerve Lesions
Optic atrophy: pallor of the optic disk, and damage to the retinal nerve layer, optic nerve or tract
leading to visual acuity or field loss. Due to neuritis, compression, ischaemia, glaucoma
Optic Neuritis: Age 18 40, more common in women. Pain on movement of eye, with central fog
patch, colour desaturation. Worsens over hours to days, may lose sight completely, gradually improves
over 4 6 weeks. 70% chance of developing MS over 10 years
Anterior Ischaemic Optic Neuropathy: Sudden painless unilateral visual loss in an older person.
Seldom improves. Due to occlusion of the arterioles to the optic nerve head
Compressive Optic neuropathy: insidious loss of central vision in one eye, especially colour. Usually
meningioma of optic nerve
Nerve Lesions Affecting Eye movement
Droopy lid (ptosis) and small pupil (Horners syndrome) due to lesions in the brain stem, in the apex
of the lung, in the neck or on the carotid artery (eg carotid dissection)
Droopy eye lid and large pupil non reactive to light: 3rd nerve palsy eye turned down and out due to
weakness of MR, SR, IO, and IR
Differential for Ptosis: idiopathic (esp elderly), myasthenia, muscular dystrophies, myotonic dystrophy
Nystagmus: if present in all directions will be central (commonest cause is antiepileptics)
Retinal Vascular Disease
Damage to large vessels in the eye
Occlusion of the central retinal artery:
Due to atheroma, thrombus, embolis, arteritis
Retina is white and totally infracted
Occlusion of the central retinal vein:
Haemorrhagic infarction
Collateral supply means some vision is recoverable
Retina is a mass of red, veins big and tortuous, cotton wool spots
Focal Ischaemic Retinal Disease
Affects little vessels
Features:
Cotton wool spots:
Fluffy and off-white/yellow
Due to micro-infarction superficial area of necrosis and oedema
Axons are disrupted and become distended (cytoid bodies)
Resolve in 6 weeks
Hard exudates:
Discrete, brighter white, often around macula
Plasma leaks from damaged capillaries (secondary to thickened basement membrane) in the
outer plexiform layer (deeper in the retina) and forms proteinaceous lakes
Resolves over several months
Haemorrhage: usually arises from microemboli/thrombi damaging vessels
Flame: a small arteriole bursts into nerve fibre layer and spreads along nerve fibres
Dot: capillary bursts into outer plexiform layer
Blot: into the subretinal space
Roths spots: central white infarct surrounded by haemorrhage
Microaneurysms:
Round or oval dilations of capillaries look like lots of very little red dots
Central in diabetes, peripheral in central retinal vein occlusion
Due to reduced numbers of pericytes surrounding capillaries
Neovascularisation:
Response of the eye to vascular insufficiency, secondary to angiogenesis factors from
ischaemia: proliferate around the margin of non-perfusion. Detect with fluorescein angiogram
Appears as fine lace work of new vessels. They leak and bleed
Sites:
Iris surface neovascular glaucoma, ectropion uvea
Pupillary membrane Posterior Synichiae
Neuro-sensory 145
Vitreal Surface haemorrhage, pre-retinal fibrovascular membranes scarring
retinal detachment
Easy to see if over optic disk (normally should only be large vessels)
Differentiating between Hypertensive and diabetic retinopathy:
Hypertensive Retinopathy Diabetic Retinopathy
Vessel Arterioles Capillaries/veins
Site Superficial nerve fibre layer Deep (non-proliferative)
Superficial (proliferative)
Pathology Medial hypertrophy Pericyte loss
BM thickening
Microaneurysms
New vessel formation
Diabetic Retinopathy
See also Diabetes Mellitus, page 94
1/3 diabetes with > 30 years disease will loose some sight. Diabetics 25 times more likely to go blind
Risk related to duration Type 1 (juvenile onset) more likely to cause damage
Retinal exam essential:
At diagnosis for maturity onset (may have had diabetes for 5 10 years)
After 5 years for juvenile onset and annually thereafter
Fluorescein angiography (injected in arm then photograph retina) to test for neovascularisation
Causes: Thickened basement membrane of retinal microcirculation leakage, oedema, nonperfusion
and micro-aneurysms
Macular retinopathy: boggy, leaky macula blurred vision
Non-proliferative retinopathy (= Background Retinopathy): Progression: oedema ( blurred vision)
microaneurysms hard exudates cotton wool spots small haemorrhages venous bleeding
Proliferative retinopathy:
Neovascularisation
Retinal detachment due to shrinkage of subsequent scars
Vitreous haemorrhage (can also be due to vitreous collapse tearing at retina or retinal venous
occlusion usually due to BP expanded artery compresses adjacent vein)
Treatment:
Regular checks
Blood sugar control
Treatment of vascular disease (eg BP)
Laser treatment (photocoagulation): 2 3,000 burns (but NEVER on macula). O2 demand
neovascularisation. Complications: peripheral and night vision, macula oedema
Vitrectomy: if non-resolving vitreous haemorrhage or fibrovascular contraction of vitreous (which
has risk of retraction of retina tear)
Retinal repair: reattach retina
Diabetes can also cause: neovascular glaucoma (blocking flow past lens), more susceptible to damage
from IOP, cataract, extraocular muscle palsy
Hypertensive Retinopathy
Rarely causes visual loss. Requires diastolic BP > 120 for many years
Stages:
Stage 0: no changes
Stage 1: copper-wiring of arterioles due to thickening of the walls due to medial thickening (very
subjective)
Stage 2: Arteriovenous nipping thickened arterioles compressing underlying veins
Stage 3: Soft-exudates and/or flame haemorrhages (spread longitudinally along fibres)
Stage 4: Papilloedema plus the above
Bilateral and symmetric. More cotton wool spots (nerve fibre hypoxia)
Retinopathy regresses if hypertension controlled (cf diabetes which doesnt)
See also Hypertension, page 34
Tumours
Can occur on the iris, ciliary body, choroids

Malignant Melanoma of the Choroid
Presentation: elderly, usually white, visual loss from retinal detachment or incidental
Retinal appearance: light to darkly pigmented ovoid, elevated mass. Many variants
2nd most common site of melanoma after the skin
Prognosis depends on cell type (Spindle A, Spindle B, Epithelioid or Mixed) and Stage. Overall 50%
at 15 years
Retinoblastoma
Life threatening
1:20,000 live births. First few years of life
Types:
60% sporadic
40% familial (90% bilateral and/or multifocal)
Presentation: strabismus (squint), white patches on papillary/red reflex (leukocoria), red eye
Pathogenesis:
Due to variety of mutations in the tumour suppressor gene RB1 at 13q14 inactivated a protein
which down regulates cell growth
Need both alleles to be mutated to cause cancer. Hereditary neuroblastoma = inherit one defective
gene from parent, with other allele in one cell undergoing spontaneous mutation. If non-
hereditary, need to acquire mutations to both alleles in one cell
Gross appearance: flat, elevated, diffuse, multicentric pale tumour nodules of plaques
Microscopic appearance: small round cells with hyperchromatic nuclei, rosettes are characteristic, areas
of necrosis and calcification
Treatment: remove eye
Complications:
Metastasis eg in CNS. From occurrence in eye to spreading down the optic track is ~ 6 months
Survivors have a 20% chance of developing malignant tumours at 10 years: osteosarcoma or
rhabdomyosarcoma
Prognosis: 90% 5-year survival (less if optic nerve invasion).
Paediatric Ophthalmology
Assessment
Vision: fixation (test independently and together), pictures, symbol matching, E
Alignment: inspection, alternating cover test
Squint inspection:
Corneal reflection when looking at bright light source. Should be in the centre of the pupil on both
sides. Cover good eye and see if corneal reflection shifts over the pupil of the bad eye
Check for equal schlera on either side of iris. Wide bridge of nose may give pseudo squint
Can have squint without amblyopia as long as brain alternates which eye it looks through. If
preference for one eye, then amblyopia
Amblyopia
= Lazy eye
Affects 2 to 3 per 100 children. Can only occur in childhood while visual pathway still developing
Usually unilateral: maybe bilateral if bad astigmatism or hypermetropia. If unilateral no effect on
reading/writing. Treat as insurance against problems in good eye
Affects central vision: peripheral vision OK
Three major causes:
Squint: Most common cause: misaligned or crossed eyes. The crossed eye is turned off to avoid
double vision
Unequal focus (refractive error). One eye is more near/far sighted or astigmatic
Visual obstruction: eg Cataract
Also caused by ocular motor defects
Treatment: force the use of the weak eye by covering the good one (for weeks or months), plus
correcting refractive errors with glasses
Refractive errors
Myopia
Neuro-sensory 147
Hypermetropia: if equal and severe then squint due to accommodation
Stigmatism
Anisometropia: difference between two eyes (especially if one normal and other long sighted)
accommodation just makes normal eye go out of focus
Other
Congenital cataract
Can be autosomal dominant
Check for red reflex within 6 weeks
May be uni or bilateral, part of a syndrome or isolated
Congenital epiphora
Watery eye. Common lacrimal system not fully developed
Spontaneous resolution the norm. Conservative treatment until 12 months. Massage +/-
antibiotics (stagnation of tear drainage)
Perinatal eye infections
Retinoblastoma: See Retinoblastoma, page 147
Retinopathy of prematurity
Very premature babies (low risk if over 30 weeks or 1200 g)
Spectrum from severe to norm
Problem with vascularisation retinal detachment over time
Congenital Glaucoma: rare. One cause of red watery eye
Vestibular
Examination of Eye Movements
Nystagmus:
Peripheral cause: fine, unidirectional, horizontal or rotatory
Beats to the side opposite the lesion, worse when looking to that side
Named for the direction of the fast phase
Is inhibited by fixation (ie will be quicker if you close one eye and try fundoscopy on the other)
Bi-directional or vertical nystagmus is always central in origin
Control of eye movement:
Saccades: voluntary quick refixation eye movement. If hypometric then undershot number of
small saccades to catch up. Hypermetric saccades overshoot reverse saccade
Parietal lobe controls ipsilateral smooth pursuit and contralateral saccades. Impairment over 70
may be normal
Impaired pursuit also due to cerebellar and brainstem lesions
Vestibulo-ocular reflexes:
Eye movements to compensate for head movement: maintain stable picture on retina
Dolls eye: eyes stay focused on target when head moves
Benign Paroxysmal Positional Vertigo (BPPV)
Usually posterior semicircular canal. Due to debris in canal (CaCO3 crystals). Usually cause unknown
or aging, but may follow trauma or infection. Fluid movement distorted stimulations to nerve due to
particles different input from 2 vestibular end organs
Posterior canals are in the snow-plough position, and are the lowest. Collect debris from the anterior
and horizontal canal
Leads to discharge to ipsilateral superior oblique and contralateral inferior rectus torsional
nystagmus
Can also be due to horizontal semicircular canal
Symptoms:
Brief attacks of vertigo precipitated by certain head movements (eg getting into or out of bed,
rolling over). Less severe when repeated
May spontaneously remit and relapse
Hallpike manoeuvre: Rotatory or torsional nystagmus beating toward affected ear when tipped
down, after a brief latent period (5 10 secs). If immediate then ?central cause. Last about 20
secs and reoccurs again when sitting up. Effect fatigues with retesting (material disperses in
process of testing)

Usually resolves over weeks or months
No cochlear symptoms
Treatment:
Drug therapy not helpful
Canalith Repositioning: induce symptoms shifts particles into a chamber not sensitive to
movement
For right ear: sit on edge of bed, turn head 45 degrees to the left, lean all the way down to the right
then quickly through 180 degrees to the left, then back to upright. May be easier with eyes closed.
Repeat after 2 3 minutes. Do every three hours
Acute Peripheral Vestibulopathy
= Acute labyrinthitis
Symptoms: acute and continuous vertigo, worse with any movement, lasting several days with nausea
and vomiting, but no auditory or neurological symptoms
Signs: unsteady walking (eg heel-toe). Fine horizontal/rotatory nystagmus beating away from the
lesion. Vestibulo-ocular reflex is absent/impaired on passive head rotation toward the lesion, requiring
voluntary eye movement to regain fixation (catch-up saccade)
Most likely to be horizontal canal affected
Other
Vertigo may follow Head injury. Eg temporal bone fracture tearing 8th nerve
Infarct with occlusion of the internal auditory artery affects hearing and balance
Chronic bilateral vestibulopathy imbalance and oscillopsia (sensation of the world moving on head
movement) due to inadequate vestibulo-ocular reflex. Usually due to gentamycin toxicity
Migraine may have vestibular symptoms
MS: vertigo is a classic feature
Ear
External Ear
Congenital Abnormalities: usually unilateral. Common ones:
Preauricular tag: only cosmetic
Preauricular sinus: get infected
Otitis Externa:
Localised: furnuncle or furnuculosis
Very painful, may abscess and discharge
Usually staph aureus
Tx: Oral antibiotics, may need drainage
Diffuse (more common)
Skin infection: viral or bacterial, or underlying dermatitis (more chronic, less pain and
swelling but itchy). If longstanding and treatment resistant, ?fungal (eg aspergillus) less
painful, but blocked and debris, look for hyphae
Treatment: swab, clean out canal, topical antibiotics (drops with steroids swelling)
Canal trauma from itching, ear cleaning. Resolves spontaneously (unless infected)
Wax: produced by suruminous glands (only in the ear) over cartilaginous part. Slightly acid
antibacterial. Carries debris out
Insect in ear. Drown it and take out at leisure
Exostosis: common benign finding. Overgrowth of bone in internal 1/3 of canal, following exposure to
cold water (surfers, divers). May obstruction
Neoplasms: on pinna: BCC or SCC require excision
Middle Ear
Middle ear cleft = ear drum + tympanum + eustachian tube
Ear drum:
Should see malleous, top towards the back
May see incus through the drum. If internal jugular very high, may see it at bottom
Main part called pars tensa, pars flaccida at top
Neuro-sensory 149
Otitis Media
See Acute Otitis Media, page 605
Other Middle Ear Conditions
Cholesteatoma:
Most commonly affects the attic (=epitympanum) and antrum of the mastoid
Pars flaccida gets sucked in, expands, erodes surrounding tissue
May present with:
Chronically discharging, smelly ear, resistant to treatment
Conductive hearing loss: ossicles eroded
Complication: brain or mastoid abscess
Treatment: remove diseased bone
Otosclerosis:
New bone formation fixes the footplate of stapes
Conductive hearing loss but ear looks normal
F > M, familial, in pregnancy, menopause
1:20 25,000K, can be bilateral
Treatment: Stapendectomy (put in piston) or hearing aid
Tympanic sclerosis. White plaques on ear drum. No consequence
Barotrauma: from flying/diving. Bleeding and bruising around malleolus. Will settle spontaneously
Haemotympanum: Blood in middle ear. ?Temporal bone fracture. Battles Sign (of temporal
fracture): bruising behind the pinna
Ear Testing
Voice Testing
Tuning fork tests:
Rinne Test: 512 Hz fork beside the ear. If conductive loss then bone conduction is better than air
conduction. If sensorineural, air conduction best
Weber Test: Tuning fork on top of the head. Louder in affected ear if conductive loss, softer in
affected ear if sensory loss
Pure Tone Audiometry:
Can establish severity of hearing impairment and whether sensorineural or conductive
Measures thresholds across a range of frequencies. Threshold = lowest intensity that can be
detected
Usually only test in range of conversational speech (250 Hz to 8 KHz)
Normal hearing is 0 20 dB (zero is based on population surveys)
Harder if child aged 3 5: need to play games etc
Auditory Brainstem Response (ABR):
Detects evoked potentials in the brainstem in response to sound
Used for neonatal testing (reliable from full term), in older kids where behavioural responses are
unclear and for testing the auditory nerve (eg acoustic neuroma but MRI is gold standard, CT
with contrast poorer)
Tympanomtery:
Measures compliance of middle ear
Normal is -100 to 100 daPa
Type A: normal (peak compliance over 0 daPa). If peak is low ?scarring or adhesions
Type B: Flat curve (ie not compliant at any pressure).
Low volume type B: wax impaction or middle ear infusion
High volume type B: perforation or grommet
Type C: Peak shifted to the left. Eustachian tube obstruction
Otoacoustic emissions:
Test for cochlear function, eg in neonatal screening
Also for tinnitis: is it cochlear or non-cochlear
Paediatric testing:
0 3 months: referred from neonatal high-risk register. Need to correct (eg hearing aid implants) by 9
10 months otherwise speech impairment
6 12 months: distraction testing looking for head turning, etc
1 2 years: in a room with speakers

Hearing Loss
See Hearing, page 580 for developmental delay resulting form hearing loss
Congenital Sensorineural Deafness
Irreversible
Pathology: problems with nerve or cochlear
Profound hearing loss at birth: 2 per 1,000
Most often detected by parents (ie believe them!)
Aetiology: genetic or acquired, etc:
Idiopathic 60%
Genetic: most are spontaneous mutations rather than family history
Low birth weight
Infection (fairly rare now), eg Rubella, also toxoplasmosis, CMV, syphilis
Maternal drugs: eg aminoglycosides, alcohol
Lots of others, eg hypoxia, high bilirubin
Sudden Onset Sensorineural Hearing Loss
=Uni/bilateral sudden onset within 3 days. May also get dizzy, tinnitis
Could be inflammatory, infective, ototoxicity, acoustic neuroma ( always investigate)
Urgent specialist referral within 24 hours
Spontaneous remission likely, poor prognosis if elderly, diabetic, vascular disease (Cochlear artery is
an end artery if blocked no collateral flow)
Presbycusis
= Age related hearing loss, especially at higher frequencies
Bilateral, symmetrical. May get recruitment (some sounds sound louder eg toilet flushing, doing
dishes)
M > F, 24% of 64 74 year olds, 40% of over 75s
May have word discrimination: hard to help, volume doesnt help
Aetiology: age, noise, hypertension, genetic predisposition
Pathology: degenerative changes, eg of cochlea and also of central procession (this part wont respond
to volume)
Clinical: progressive deafness, social deafness, especially 1 KHz, tinnitis. Often judged worse by
spouse/partner
Exclude: wax impaction, otosclerosis, Pagets disease of the middle ear bones, acoustic neuroma
Management:
Screen elderly people (eg questionnaires or audiometry)
Hearing aid: only who would benefit use one, although there are many barriers to use (including
cost)
Speaking facing the person, clearly, slowly, not too loud, paraphrasing sentences that arent heard
rather than repeating them (also give this advice to spouse and caregivers),
Aids (telephone boosters, lights that flash when the doorbell rings, etc)
Rehabilitative services available through the Hearing Association
Noise Induced Hearing Loss
Commonest cause of hearing loss < 60
Usually industrial noise exposure: factories, builders, firearms, jack hammers
Safe limit: 80 db for not more than 4 hours
Classic damage at 4 & 6 KHz on audiogram. Usually bilateral
Treatment: Prevention, hearing aids not much help
Menieres Disease
Diagnostic triad: tinnitus (usually low pitched), deafness, vertigo, (+ feeling of aural fullness)
Clinical: acute onset of triad, disabling vertigo (world spinning, vomiting) for 6 12 hours then low
frequency hearing loss
30 55 years, M > F
Stages:
Early: occasional attacks
Later: fluctuating low tone deafness
Neuro-sensory 151
End stage: low tone deafness, imbalance but no vertigo
Pathology: endolymphatic hydrops: distension of endolymphatic space
Aetiology: unknown. ?Production of endolymph
Diagnosis: possibly nystagmus, fluctuating SN loss
Treatment: Supportive, low Na diet (endolymph), thiazides, antivertigo, antiemetic and histamine
medication
Acoustic Neuroma
Progressive loss of hearing in one ear with tinnitus.
Not usually associated with vestibular function slow enough to compensate (ie CNS adjusts so
world doesnt seem on a tilt). But, everyone with acute vertigo should have a pure tone audiogram to
screen for the (rare) possibility of acoustic neuroma
MRI is definitive, CT is unreliable and should not be done
Aural Rehabilitation
When hearing loss cannot be corrected, use hearing aids, listening devices and communication
strategies

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Neurology ....................................................... 117

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Basal Pontine Abducens Ipsilateral medial deviation of the

Mediobasal Oculmotor Ipsilateral outward deviation of eye

Transient Ischaemic Attacks (TIAs):

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Haemorrhagic infarct Intracerebral Haemorrhage

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Conventional drugs have hepatic clearance

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