A stroke is defined by the WHO as the rapid development of clinical signs of cerebral dysfunction, with signs lasting at least 24 hours or leading to death with no apparent cause other than that of vascular origin.¹

About 795,000 Americans suffer a new or recurrent stroke. This means that, on average, a stroke occurs every 40 seconds. Stroke kills more than 137,000 people a year, which is about 1 of every 18 deaths. It is the No. 3 cause of death behind diseases of the heart and cancer. On average, every 4 minutes, someone dies of stroke. About 40% of stroke deaths occur in males and 60% in females. The 2006 US stroke death rates per 100,000 population for specific groups were 41.7 for white males, 41.1 for white females, 67.7 for black males, and 57.0 for black females.

The two major types of stroke are ischemic (≈83%) and hemorrhagic (17%).² On further categorizing, 32% are embolic, 31% large vessel thrombotic, 20% small vessel thrombotic, 10% intracerebral hemorrhagic, and 7% subarachnoid hemorrhagic.² The Framingham Heart Study data revealed 30-day survival rates to be 73% to 81% following cerebral infarction and 36% after intracerebral hemorrhage,³ although survival figures vary widely in the literature and have generally been improving with time.

Males, African Americans, and the elderly are at increased risk for developing stroke. Modifiable risk factors include HTN, DM, hypercholesterolemia, hyperhomocysteinemia, hypercoagulable states, heart disease, carotid arteriosclerosis, substance abuse, obesity, and a sedentary lifestyle.

MCA – Deficits can include c/l hemiplegia/hypesthesia (face and arm worse than leg), c/l homonymous hemianopia, and i/l gaze preference.

With dominant hemisphere involvement, receptive aphasia (inferior division of MCA to Wernicke’s area) and/or expressive aphasia (superior division of MCA to Broca’s area) can occur, but classically patients can learn from demonstration and mistakes. Gerstmann’s syndrome (parietal lobe) consists of asomatognosia (right-left confusion), dyscalculia, finger agnosia, and dysgraphia.

With nondominant hemisphere involvement, spatial dyspraxia and c/l hemineglect may be seen; insight/judgment are often affected (likely to need supervision); ADL recovery is often said to be slower.

Acrodermatitis Chronica Atrophican (ACA) – Deficits can include c/l hemiplegia/hypesthesia (leg worse than arm; face and hand spared), alien arm/hand syndrome, urinary incontinence, gait apraxia, abulia (inability to make decisions), perseveration, amnesia, paratonic rigidity (Gegenhalten, or variable resistance to passive ROM), and transcortical motor aphasia (with a dominant hemisphere ACA lesion).

Posterior Cerebral Artery (PCA) – Deficits can include c/l homonymous hemianopia, c/l hemianesthesia, c/l hemiplegia, c/l hemiataxia, and vertical gaze palsy. Dominant-sided lesions can lead to amnesia, color anomia, dyslexia w/o agraphia, and simultagnosia (defunct perceptual analysis). Nondominant-sided lesions can lead to prosopagnosia (cannot recognize familiar faces).

The central poststroke pain (Dejerine-Roussy or thalamic pain) syndrome can occur with involvement of the thalamogeniculate branch. Weber’s syndrome (penetrating branches to the midbrain) consists of i/l CN III palsy and c/l limb weakness). A b/l PCA stroke can cause Anton syndrome (cortical blindness, with denial) or Bálint’s syndrome, which consists of optic ataxia, loss of voluntary but not reflex eye movements, and an inability to understand visual objects (asimultagnosia).

Brain Stem – The lateral medullary (Wallenberg) syndrome (posterior inferior cerebellar artery) consists of vertigo, nystagmus, dysphagia, dysarthria, dysphonia, i/l Horner’s syndrome, i/l facial pain or numbness, i/l limb ataxia, and c/l pain and temporary sensory loss. The “locked-in” syndrome (basilar artery) is due to b/l pontine infarcts affecting the corticospinal and bulbar tracts, but sparing the reticular activating system. Patients are awake and sensate, but paralyzed and unable to speak. Voluntary blinking and vertical gaze may be intact. The Anton syndrome (basilar artery) is characterized by cortical blindness with denial. The Millard-Gubler syndrome is a unilateral lesion of the ventrocaudal pons that may involve the basis pontis and the fascicles of cranial nerves VI and VII. Symptoms include contralateral hemiplegia, ipsilateral lateral rectus palsy, and ipsilateral peripheral facial paresis. When the penetrating branches of the PCA to the midbrain get affected, it could result in Weber syndrome. Symptoms are ipsilateral characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.

Lacunar – The more common syndromes include pure motor hemiplegia (posterior limb internal capsule [IC]), pure sensory stroke (thalamus or parietal white matter), the dysarthria-clumsy hand syndrome (basis pontis), and the hemiparesis-hemiataxia syndrome (pons, midbrain, IC, or parietal white matter). “Pseudobulbar palsy” is caused by anterior IC and corticobulbar pathway lacunes (loss of volitional bulbar motor control [e.g., dysarthria, dysphagia, dysphonia, and face weakness], but involuntary motor control of the same muscles is intact, e.g., can yawn or cough). Emotional lability may be seen.