Medicine Simplified DBMCI

Chapter-3
Neurology

Spinal Cord (Ref. Harrison 20th ed. pg. 3172)

Basic Concepts
Anatomy
1. It extends from the foramen magnum in the skull to the lower border of first lumbar vertebrae.
2. Filum terminale – A fibrous extension of conus medullaris that terminates at the coccyx.
3. Conus medullaris – Below lumbar enlargement the spinal cord narrow and ends as conus medullaris.
4. Cauda – equina – The lumbar roots from L2 and sacral roots congregate around the filum terminale and form cauda.
equina.
5. Cervical enlargement C5 – T1, widest at C6 – Due to formation of brachial plexus.
6. Lumbar enlargement L3 – S2 widest at S1 – Due to formation of lumbosacral plexus.

Blood Supply : Spinal cord is supplied by one ant. spinal artery (ant. 2/3) and a pair of post. Spinal arteries (post 1/3)
Sensations Transmitted by Posterior / Dorsal Column
1. Fine Touch (Sensations requiring fine gradients of intensity / high degree of localization (NEET 2017)

Neurology - Chapter-3
2. Fine Pressure (Fine degrees of judgment of pressure intensity)
3. Vibration
4. Joint Position Sense
Sensations Transmitted by Anterolateral Column / Spinothalamic Tract
1. Crude Touch 2. Crude pressure 3. Pain (Pin Prick) 4. Temperature (NEET 2017)

Important Point: Fine touch are transmitted by the Posterior column.

Spinal cord had 31 pairs of spinal nerves.

Table - Spinal Cord Levels Relative to the Vertebral Bodies
Vertebral column Spinal cord segment
Cervical Add 1
T1 – T6 Add 2
T7 – T9 Add 3
T10 L1 – L2
T11 L3 – L4
T12 L5
L1 Sacral & coccygeal

Segmental levels of some common reflexes include:

Deep Superficial
Ankle jerk: S1, S2 Triceps jerk : C 7,8 Plantar reflex : S1, S2
Knee jerk: L3,4 Radial jerk : C 6 Abdominal reflex : T7 - T11 Cremasteric
Biceps jerk: C5, 6 Jaw Jerk : Pons reflex : L1

Beevor’s sign (NEET 2016)

1. It is characteristic of spinal cord injury between T6 and T10 levels.

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2. This occurs because the upper abdominal muscle such as the Rectus Abdominus are intact at the top of the abdomen
but weak at the lower portion. Thus when the patient is asked to do a sit up only the upper muscles contract pulling
the umbilicus toward the head in patients who are abnormal.
3. It is also seen in amyotrophic lateral sclerosis and Facioscapulohumeral muscular dystrophy.

Demonstrating Beevor’s sign

Brown Séquard Syndrome

Brown Séquard syndrome (Hemisection of the cord) (NEET 2018)
1. Sensations lost on the same side as the lesion (Ipsilateral posterior column involvement)
a. Vibration
b. Joint Position (Proprioception)

Neurology - Chapter-3
c. Fine touch
2. Motor power is lost on the same side as that of the lesion (Ipsilateral corticospinal tract involvement)
3. Sensation lost on the opposite side of lesion (Contralateral spinothalamic tract involvement).
a. Touch (Crude touch) b. Pain c. Temperature

Diseases Involving Spinal Cord

1. Spinal cord compression

a. Cervical spondylosis b. Cervical or thoracic disc
c. Metastatic tumor d. Primary tumor (meningioma, neurofibroma etc)
e. Infective (epidural abscess, spinal TB etc) f. Epidural haematoma
2. Inflammatory disorders
a. Multiple sclerosis b. Idiopathic transverse myelitis
c. Sarcoidosis d. Infections (Lyme, zoster, TB, AIDS)
3. Degenerative disorders
a. Motor neuron disease b. Syringomyelia
4. Vascular
a. Spinal cord infarction b. Vasculitis, systemic lupus erythematosus etc
c. Spinal AVM
5. Trauma Metabolic/Nutritional
a. Cord contusion, laceration or transaction b. Displaced vertebral fracture or disc
c. Traumatic epidural hematoma
6. B12 deficiency (subacute combined degeneration)
7. Rare hereditary conditions
a. Friedreich ‘s ataxia Hereditary spastic paraparesis

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8. Parasagittal brain lesions

a. Meningioma b. Cerebral venous sinus thrombosis

Syringomyelia

1. Syringomyelia is a cavitatory expansion of central

canal of spinal cord caused by chronic progressive
destruction of it’s Grey & White matter.
2. The most commonly involved regions are
the ‘Lower cervical’ and ‘upper thoracic’.( Cape like
distribution of deficit)
3. It involves the sensory fibres, which cross the
midline to form the spinothalamic tract.
4. As these fibres carry the sensations for temperature
& pain, one of the earliest signs of disease is an
inability to differentiate or appropriate ‘Hot and
Cold’ sensations on the inner side of forearm and
hand.
5. Thermo-anaesthesia usually precedes
the Analgesia while Touch sensitivity is usually
preserved (This leads to Multiple burns and non
healing ulcers over the hands and forearms)

Neurology - Chapter-3
6. This particular form of “sensory loss” to
temperature & pain with sparing of touch, is
described as ‘Dissociate Anaesthesia’ and is
considered as the “True Hallmark of the disease”.
(NEET 2017)
7. Most accurate test: MRI - Bubble in cord

Syringomyelia

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Treatment: Syringomyelia
1. Treatment of syringomyelia is generally unsatisfactory.
2. The Chiari tonsillar herniation is usually decompressed, generally by suboccipital craniectomy, upper cervical
laminectomy, and placement of a dural graft.
3. Syringomyelia secondary to trauma or infection is treated with a decompression and drainage procedure in which a
small shunt is inserted between the syrinx cavity and the subarachnoid space; alternatively, the cavity can be
fenestrated.

Anterior Spinal Artery Thrombosis/Syndrome

1. Anterior Spinal Artery is a single artery that supplies the anterior two thirds of the spinal cord.
2. Sparing of posterior column
Posterior 1/3” of the cord is supplied by the posterior spinal artery and hence the posterior column is spared and
vibration &joint position sense are preserved
3. Pain at site of infarction
Moderate to severe back pain at the site of cord infarction, most often in the thoracic region.
4. Infarction of the corticospinal tract
a. Paraplegia with UMN signs (Spasticity and hyper-reflexa)
5. Infarction of the anterolateral tracts (spinothalamic tract)

Neurology - Chapter-3
a. Loss of pain and temperature sensation distal to the lesion
6. Infarction of the fibres required for sphincter control (carried in anterior 2/3rd of cord)
a. Loss of bladder control

Spinal Cord Compression

Table: Causes of spinal cord compression.
Site Frequency Causes
Vertebral (Extradural) 80% Intravertebral disc prolapse, Trauma Secondary from Breast,
Bronchus, Prostate, Myeloma, Tuberculosis
Meninges (Intradural) 15% Tumours, Meningioma, Neurofibroma, Ependymoma,
(extramedullary) Metastasis, Lymphoma, Leukaemia, Epidural abscess
Spinal cord (intradural 5% Tumours Glioma, Ependymoma, Metastasis
intramedullary)
(Pain due to spinal stenosis is worse while walking down the hill because of body leaning back)

Lesions at various sites of Spinal Cord

1. Above the fifth cervical segment – upper motor neurone signs and sensory loss of all four limbs;
2. Between fifth cervical and first thoracic – lower motor neurone signs and segmental sensory loss in the arms and upper
motor neurone signs in the legs; Thoracic cord – spastic paraplegia with a sensory level on the trunk;
3. Lumbosacral cord and cauda equina – lower motor neurone signs and segmental sensory loss in the legs. The spinal
cord ends at approximately the T12/L1 spinal level and spinal lesions below this level can only cause lower motor
neuron signs.
4. The Brown-Séquard Syndrome results if damage is confined to one side of the cord. On the side of the lesion there is
a band of hyperesthesia with below it loss of proprioceptive sense and upper motor neurone signs. On the other side
there is loss of spinothalamic sensation (pain, temperature) as fibers of that tract decussate soon after entering the
cord.

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Comparison of Intramedullary and Extramedullary Compression

1. Symptoms Intramedullary Extramedullary

a. Root pain Uncommon Common
b. Vertebral pain Uncommon Common
c. Muscle Weakness Uncommon Common
d. Sacral Involvement (NEET 2016) Late Early
2. Signs
a. Brown Séquard Uncommon Common
b. Dissociative sensory loss Present Absent
c. Bladder/ bowel dysfunction Late Early
3. Investigation –
Subarachnoid Block Late & less marked Early & marked

Extra medullary Spinal Cord Compression:

Neurology - Chapter-3
1. Acute and chronic conditions characterized by external mechanical compression of the SPINAL CORD due to
extramedullary neoplasm; EPIDURAL ABSCESS; SPINAL FRACTURES; bony deformities of the vertebral bodies; and
other conditions.
2. Clinical manifestations vary with the anatomic site of the lesion and may include localized pain, weakness, sensory
loss, incontinence, and impotence.

Extra Edge
1. A Hoffmann (or Tinel's sign) is a tingling sensation triggered by a mechanical stimulus in the distal part of an injured
nerve.
2. This sensation radiates peripherally, from the point where it is triggered to the cutaneous distribution of the nerve.
3. The tingling response can be compared with that produced by a weak electric current, as in transcutaneous electrical
nerve stimulation (TENS).
4. This unpleasant sensation is not a severe pain and does not persist

Conus Medullaris Syndrome

a. The conus medullaris is the tapered caudal termination of the spinal coral, comprising the sacral and single coccygeal
segments.
b. The distinctive conus syndrome consists of bilateral peri anal anesthesia (S3-S5), prominent bladder and bowel
dysfunction (urinary retention and incontinence with lax anal tone), and impotence.
c. The bulboncavernom (S2-S4) and anal (S4-S5) reflexes are absent.
d. Muscle strength is largely reserved.
e. Mass lesions in the lower spinal canal often produce a mixed clinical picture with elements of both cauda equina and
conus medullaris syndromes.
Cauda Equina Syndrome
a. It signifies an injury of multiple lumbosacral nerve roots within the spinal canal distal to the termination of the spinal
cord at L1-L2.
b. Low back pain, weakness and areflexia in the legs.
c. Saddle anesthesia, or loss of bladder function do not occur or occur as late feature.

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d. The problem must be distinguished from disorders of the lower spinal cord (conus medullaris syndrome), acute
transverse myelitis and GBS.

Differences between Conus Medullaris Syndrome and Cauda Equina Syndrome

Conus medullaris Cauda equina
1. Root involved S3, S4, S5, L2 – L4
2. Root pains - uncommon Common
3. Involvement - B/L U/L
4. Symmetry - Symmetrical Asymmetrical
5. Site - Perineum Thigh / leg
6. Motor Signs - Usually no weakness Asymmetric weakness
7. Knee reflex - Present Absent
8. Ankle reflex - Absent Present
9. Sensory – - Peri anal anesthesia Saddle anesthesia
10. Bladder / bowel - Early & marked (NEET 2017) Late, less marked
Note: Conus medullaris syndrome is a very important DD of BHP. But in BHP there is no loss of peri anal sensation and
ankle jerk is normal.

Spastic Paraplegia

Neurology - Chapter-3
1. Cervical spinal cord injury
2. Decompression sickness
3. Infectious Disorders (Specific Agent)
a. HIV b. Syphilis c. Potts paraplegia/Epidural cold abscess d. Tabes dorsalis
4. Infected organ, Abscesses
a. Spinal epidural abscess
5. Neoplastic Disorders
a. Cervical / Thoracic spinal cord tumor b.Metastasis to spinal cord
c. Intraspinal tumor d. Spinal Meningioma e. Multiple Sclerosis
6. Deficiency Disorders
a. Copper deficiency b. Vitamin B12 deficiency (Subacute combine degeneration)
7. Congenital, Developmental Disorders
a. Congenital narrow neural canal/Cervical b. Syringomyelia
8. Hereditary, Familial, Genetic Disorders
a. Hereditary spastic Paraplegia b. Friedreich’s ataxia c. Hereditary Spinocerebellar ataxia
type I
9. Anatomic, Foreign Body, Structural Disorders
a. Spondylosis, cervical b. Cervical spinal stenosis c. Parasaggital Brain Lesion
10. Drugs
a. Nitrous oxide (N2O) Administration/Toxicity/abuse
11. Poisoning (Specific Agent)
a. Lathyrism

Note: In lead poisoning it resembling radial neuropathy, Autonomic Neuropathy & blue line in gum (Burton lines)

Transverse Myelitis
1. Causes.
a. Immunological – Post infections – Influenza, measles, varicella, rubella, mumps, EBV, CMV, Mycoplasma
b. Post vaccine – rabies, influenza

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c. Demyelination – MS
d. Connective tissue disorders – SLE, Sjögren’s syndrome, Behçet’s disease, sarcoidosis.

2. Diagnostic criteria –
a. Acute/Subacute onset
b. Truncal sensory level
c. Absence of other known neurological disease
d. Lack of progression over 4 weeks
e. Motor, Sensory & Sphincter disturbances
f. No clinical/ lab evidence of cord compression

3. Clinical features
a. Most common site upper/ mid thoracic cord
b. Initial symptom focal back pain/ neck pain.
c. Paresthesia, sensory, motor, sphincter disturbances within hours to days.
d. Areflexia initially → Hyperreflexia.
CSF – Pleocytosis, Proteins mildly increase.
4. Poor prognosis –
a. Spinal shock
b. Severe back pain

Neurology - Chapter-3
5. Treatment – I.V. Methyl Prednisolone followed by oral prednisolone

Cranial Nerve

Basic Concepts
1. Pure motor cranial nerves – III, IV, VI, XI, XII
2. Pure sensory - I, II, VIII
3. Mixed - V, VII, IX, X.

Olfactory Nerve
Lesions
1. Anosmia → Absence of ability to smell – Kallmann syndrome (NEET 2019)
2. Hyperosmia → Increased sensitivity to smell – migraine, Addison’s diseases, hyperemesis gravida

Extra Edge:
1. Olfactory is the only sensory modality which has no thalamic connection.
2. Kallmann syndrome = Anosmia + congenital deficiency of hypothalamic gonadotrophic hormone. Which causes
infertility.

Second Cranial Nerve

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Localization –

Fig: Visual pathways and field detects.

Neurology - Chapter-3
Lesions in optic pathway
1. Compression of chiasma Bitemporal hemianopia
2. Optic tract lesion C/L Homonymous hemianopia
3. Lesions in optic radiation in temporal lobe Superior quadrantic homonymous hemianopia (Meyer’s loop)
4. Lesions in optic radiation in parietal lobe Inferior quadrantic homo. homonymous
5. Occipital cortex 1. Homonymous hemianopia with macular sparing.
2. Cortical blindness
Note: In Right optic tract lesion there is left homomymous hemianopia

IIIrd Nerve

Lesions affecting IIIrd Nerve –

Site -Midbrain

1. Weber’s syndrome (NEET 2016): ipsilateral 3rd nerve palsy + contralateral hemiparesis (NEET 2016)

2. Nothnagel syndrome : Ipsilateral 3rd nerve palsy + contralateral cerebellar signs

3. Benedikt’s syndrome :Ipsilateral 3rd nerve palsy + Contralateral cerebellar signs

4. Claude syndrome : Benedikt’s + Nothnagel syndrome (NEET 2018) (I/L 3rd Nerve Palsy + C/L cerebellar signs)

5. Dorsal mid brain syndrome :Parinaud’s syndrome : (Loss of up gaze, lid retraction, Skew deviation)

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Cortico
Spinal
3rd Nerve Tract Weber Syndrome
Red
Nucleus

Benedict
Syndrome

Neurology - Chapter-3
Cut Section of brain at mid brain level

Transverse section of the Pons at level of Facial Colliculus

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Cut Section at Pons level

Pontine Syndromes

1. Ventral pontine syndrome (Millard Gubler syndrome) (NEET 2020)

Caused by paramedian infarction of pons
a. Ipsilateral paresis of lateral rectus with diplopia (damage to abducent Nerve)
b. Ipsilateral paresis of upper and lower face (damage to 7th cranial nerve)
c. Contralateral hemiplegia with sparing of contralateral face (damage to corticospinal tract)

2. Lower dorsal pontine syndrome (Foville's syndrome)

Caused by lesion in dorsal tegmentum of lower pons
a. Ipsilateral horizontal gaze palsy (damage to nucleus of abducent nerve and paramedian pontine reticular
formation.)
b. Ipsilateral paresis of whole face (damage to nucleus and fibers of 7th nerve)
c. Contralateral hemiplegia with sparing of Contralateral face (damage to corticospinal tract)

3. Upper dorsal pontine syndrome (Raymond Ceston syndrome)

Caused by obstruction of long circumferential branches of basilar artery
a. Ipsilateral ataxia and coarse intention tremor (damage to superior and middle cerebellar peduncle)
b. Ipsilateral paralysis of muscles of mastication and sensory loss in face. (damage to sensory and motor nuclei and

Neurology - Chapter-3
tracts of CNS)
c. Contralateral loss of sensory modalities in the body (damage to spinothalamic tract and medial lemniscus)
d. Contralateral hemiparesis of face and body (damage to corticospinal tract) may occur with ventral extension of
lesion.
e. Horizontal gaze palsy may occur (as in lower dorsal pontine syndrome)

Locked – In – syndrome (Bilateral ventral pontine lesion)

1. Locked-in syndrome is also known as cerebromedullospinal disconnection, de-efferented state, pseudocoma, and
ventral pontine syndrome.
2. Locked-in syndrome is a condition in which a patient is aware and awake but cannot move or communicate verbally
due to complete paralysis of nearly all voluntary muscles in the body except for the eyes.
3. Able to communicate only by vertical eye movement and blinking but otherwise is completely immobile)
4. Occurs in patients will bilateral ventral pontine lesion
5. Its most common cause is pontine infarction.
6. Patient
a. Is quadriplegic (bilateral damage to corticospinal tract in ventral pons
b. Is unable to speak and incapable of facial movements (involvement of corticobulbar tracts)
c. Has limited Horizontal eye movements (bilateral involvement of nuclei and fibres of 6th CN)
d. No vertical eye movements and blinking (supranuclear ocular motor pathways are spared)
e. Has preserved consciousness (reticular formation is not damaged)

Extra Edge: Blink reflex is used for mid-pontine lesion. (AIIMS Nov 2017)

Lesion affecting VI nerve

Site/ Pone
Pons Millard – Gubler synd = ipsilateral VI, VII palsy + C/L hemiparesis
Foville’s syndrome = lat. gaze palsy, ipsilateral VI, VII, palsy, C/L hemiparesis

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V Cranial Nerve (Trigeminal Nerve) (Ref. Harrison 20th ed. Pg. 3166)
Anatomy (Basic concepts)
1. Sensory system –
a. Ophthalmic div – forehead, nose.
b. Maxillary div – Malar region, upper lip
c. Mandibular div – Chin. lower lip
2. Motor system – Masseter ms. Temporalis ms. Pterygoid ms.
3. Reflexes –
a. Corneal reflex – Receptor → Free nerve ending (pain)
Afferent →Trigeminal nerve Efferent→Facial nerve
This reflex lost in any lesion involving this reflex arc. Also lost in lesion of parietal lobe.
b. Jaw Jerk – Exaggerated in pseudobulbar palsy.
c. Blink reflex/ glabellar reflex/ orbicularis oculi reflex.
Aff – Trigeminal nerve Eff – Facial nerve

Clinical features –
1. Nuclear lesion→
a. This occur due to diseases affecting pons, medulla and upper cervical cord upto C 2
b. Causes
Tumour, Demyelination, Vascular lesion, Syringomyelia, Syringobulbia.

Neurology - Chapter-3
2. Pontine lesion – Ipsilateral atrophy and weakness of the muscles of mastication along with ipsilateral facial
sensoryloss with C/L hemiplegia.
3. Lower medulla & upper cervical cord
a. Ipsilateral loss of pain and temp. over the face and C/L hemiplegia.
b. Causes – Tumour, abscess, Herpes zoster.
c. It is associated with a number of complications like pain, uveitis, keratitis and corneal perforation.

4. Reader’s paratrigeminal syndrome –

a. This results due to lesion close to the Gasserian ganglion.
b. It is characterized by unilateral Horner’s syndrome without facial anhidrosis (as the pseudomotor fibres to the face
are not involved) and ipsilateral loss of facial sensation.

5. Post ganglionic lesions –

Causes –
a. cavernous sinus lesion (III, IV, VI also) b. Gradenigo’s syndrome (ophth + Max div. + VI + Retrobulbar pain)

Petrous apex Mastoiditis - Gradenigo’s syndrome = Deafness, diplopia, headache, Ipsilateral VI palsy
Cavernous sinus Thrombus III, IV, V, VI, N lesion

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