Postictal Todds Paralysis Associated with Focal Cerebral

Hypoperfusion on Magnetic Resonance Perfusion Studies

Hussam A. Yacoub, DO, MS, Nathan Fenstermacher, PA, and John Castaldo, MD
Department of Medicine, Division of Neurology, Lehigh Valley Health Network, Allentown, PA

Abstract
BackgroundThe exact underlying physiology of postictal motor deficits, known as Todds paralysis, is
not well understood and its vascular perfusion physiology is not well studied. Reversible postictal perfusion
abnormalities have been sparsely described in the literature.
Journal of Vascular and Interventional Neurology, Vol. 8

MethodsWe report abnormal brain magnetic resonance perfusion maps in a 9-year-old boy who presen-
ted with postictal left hemiparesis. This case correlates postictal hemispheric cerebral hypoperfusion with
clinical evidence of Todds paralysis.
ConclusionsOur case provides an insight into the potential pathophysiology mechanism underlying
Todds paralysis and the practicality of magnetic resonance perfusion studies in localizing an epileptogenic
zone in the postictal patient.

Keywords
focal cerebral hypoperfusion; magnetic resonance; postictal Todds paralysis

Case Report tory included insulin-dependent juvenile-onset diabetes

mellitus and attention deficit disorder. Medications used
A right-handed, 9-year-old boy with juvenile-onset dia- included insulin, methylphenidate, and risperidone.
betes was brought to our pediatric emergency depart-
ment by his grandmother for the acute onset of stroke- On initial evaluation, the patient was afebrile with a
like symptoms. The boy had awoken that day with blood pressure of 112/84, pulse of 114 beat per minute,
newly discovered left hemiparesis unassociated with and 100% oxygen saturation on room air. He was awake,
confusion, dysarthria, or aphasia. Immediate finger stick alert, and oriented to name, age, and place. He had the
revealed a glucose level of 78 mg/dL, and the left hemi- mentation, intellect, and judgment of a nine-year-old
paresis did not improve with sugar ingestion. A code child. Pupils were equal and reactive to light and extra-
stroke was called for emergency neurological interven- ocular muscles were intact. Funduscopic and visual field
tion with the potential use of thrombolytics. examination were unremarkable. No facial weakness
was appreciated. Motor examination was normal except
Further history revealed that the boy had three spells for a mild left arm and leg hemiparesis rated at 5/5.
prior to this presentation that were clinically suspicious Muscle bulk and tone were normal as were the sensory,
for complex partial seizures. All events were witnessed coordination, and gait examinations.
by family and described as word-salad aphasia followed Laboratory studies revealed a WBC of 4,400/L, plate-
by confusion lasting for approximately 2 minutes. He lets 302,000/L, sodium 142 mEq/L, potassium
was evaluated by a pediatric neurologist, and the diagno- 4.7 mEq/L, glucose 105 mg/dL, and serum creatinine
sis of seizures was entertained, but no antiepileptic med- 0.5 mg/dL.
ications were prescribed. An electroencephalogram
(EEG) revealed left hemispheric slowing but no epilepti- Magnetic resonance imaging (MRI) of the brain showed
form activity. After 2 weeks, during follow-up, 48-hour no areas of restricted diffusion. There was evidence of
video EEG monitoring and magnetic resonance imaging mild cortical edema in the right frontal region involving
(MRI) of the brain were normal. The past medical his- the middle and anterior cerebral arteries vascular terri-

Vol. 8, No. 2, pp. 3234. Published April, 2015.

All Rights Reserved by JVIN. Unauthorized reproduction of this article is prohibited
Corresponding Author: Hussam A. Yacoub, DO, MS, 1250 South Cedar Crest Blvd, Suite 405, Allentown, PA 18103. [email protected]
 Yacoub et al. 33
Journal of Vascular and Interventional Neurology, Vol. 8

Figure 1. Magnetic resonance perfusion maps demonstrated decreased relative cerebral blood volume (a) and flow (b)
with a corresponding increase in the mean transient time (c) in the right frontal region involving the middle and ante-
rior cerebral arteries vascular territory.

Figure 2. Magnetic resonance perfusion maps obtained 24 hours after the initial study demonstrated symmetrical rela-
tive cerebral blood volume (a) and flow (b), and mean transient time (c) in the right frontal region involving the middle
and anterior cerebral arteries vascular territory.

tory (images not shown). The conventional images dem- An EEG showed focal delta slowing over the right fron-
onstrated a very subtle T1 hypointensity and T2 hyperin- tal region. The patients left hemiparesis improved to
tensity in the right frontal cortex but no abnormal normal within 2 hours of presentation. A follow-up
enhancement. A magnetic resonance angiogram (MRA) MRP completed approximately 24 hours from the initial
of the head showed diminution in the caliber of the dis- presentation showed total resolution of the abnormal
tal right internal carotid artery and decreased flow in the perfusion maps (Fig. 2) and susceptibility in the right
distal branches of the right middle and anterior cerebral frontal sulci.
arteries (images not shown), but an immediate follow-up
The patient was started on levetiracetam and discharged
percutaneous 4-vessel cerebral arteriography was unre-
home in a stable condition.
markable. Magnetic resonance perfusion (MRP) maps
demonstrated abnormally decreased regional cerebral
blood volume (rCBV) and flow (rCBF) with a corre- DISCUSSION
sponding increase in the mean transient time (MTT) in Postictal motor deficits, known as Todds paralysis, have
the right frontal lobe involving the middle and anterior been described as early as the 1800s, [1] but its exact
cerebral arteries vascular territory (Fig. 1). underlying pathophysiology is still not well understood
 34

and vascular perfusion physiology is not well studied. is distinctive because a marked increase in the mean
Reversible postictal perfusion abnormalities have been transient time did not correlate with a large vessel steno-
sparsely described in the literature. Most case reports of sis. We therefore advise caution when interpreting MRP
reversible MRI findings cite increase in T2-weighted parameters when the clinical presentation is most consis-
signals, increased rCBV, decreased apparent diffusion tent with a seizure and a postictal state. A decrease in
coefficient (ADC) mapping, coupled with hyperperfu- cerebral blood flow and volume, along with an increase
sion in the postictal state. Hassan et al. [2] reported two in MTT, is a pattern that typically denotes cerebral
cases of postictal paresis associated with computed infarct rather than a metabolic disturbance or a seizure.
tomography perfusion evidence of increased cerebral Careful interpretation and correlation of this data with
blood flow and volume and decreased mean transient the clinical presentation, EEG findings, previous history,
time in the vascular territory corresponding to patients and lack of vascular risk factors may avoid unnecessa-
symptoms. These changes are believed to be in response rily revascularization procedures in the postictal patient.
to hypermetabolic neuronal activity from seizure dis- Our case further provides an insight of the potential
charges and can be differentiated from ischemia by the pathophysiology mechanism underlying Todds paraly-
Journal of Vascular and Interventional Neurology, Vol. 8

finding of increased perfusion. [35] Hypoperfusion has sis and the practicality of MRP studies in localizing an
rarely been reported and when seen has occurred later in epileptogenic zone in the postictal patient.
the postictal phase and after an initial period of hyper-
perfusion. [6,7] References
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MTT is a sensitive indicator of acute cerebral ischemia

secondary to large vessel stenosis or occlusion. Our case