V Lecture-Neurology-Stroke. Walenberg Syndrom. Spinocerebellar Ataxia

V LECTURE
STROKE
WALENBERG SYNDROM
SPINOCEREBELLAR ATAXIA
Lecturer: Ekaterine Mamukelashvili

Overview
Stroke is a general term that implies damage to cerebral tissue from
abnormalities of the blood supply.
In simple terms, there may be insufficient blood to the brain (ischemic stroke
or infarction), abnormal excess blood (hemorrhagic stroke or cerebral
hemorrhage), or inadequate venous drainage of cerebral blood (venous stroke).
Ischemic strokes represent 85% of all strokes, hemorrhagic strokes 14%, and
venous strokes 1% (Table 9-1).
Stroke is the third-leading cause of death in the United States. Each year
500,000 people in this country develop a stroke and 150,000 die.
Pathophysiology
Cerebral ischemia occurs from inadequate cerebral blood flow to a brain area.
Total lack of oxygen and glucose to all brain neurons, as in a 12-to-15 second
cardiac arrest, suppresses electrical activity and causes loss of consciousness.
Normally cerebral arterial blood flow is 50 mL/100 g of brain per minute. When
cerebral blood flow falls below 18 mL/100 g of brain per minute, cerebral
function falters but neurons may remain alive. Thus, electrical activity ceases and
sodium/potassium pumps begin to fail, but the neurons are viable and can
recover function if blood flow improves. In a stroke, this area of potential
recovery is called an ischemic penumbra. Blood flow below 8 mL/100 g of brain
per minute results in neuronal death as early as 15 minutes after flow disruption.
Neurons in the hippocampus and cerebellum are the most sensitive to ischemia,
while neurons in the brainstem and spinal cord are the most resistant. Brain
ischemia results in impaired energy metabolism, with accumulation of calcium
ions in the intracellular space, elevated lactate levels, acidosis, and production of
free radicals. Cellular homeostasis is disrupted, leading to neuronal death.
Stroke from occlusion of a specific cerebral artery causes a wedge-shaped
infarction (Figure 9- 1). If a large artery occludes, such as the middle cerebral
artery, the stroke may involve that entire vascular territory, or portions may be
spared depending on the degree of collateral circulation. With global
hypotension, anoxia, or hypoglycemia, the stroke maximally involves the
watershed territory between the middle and posterior cerebral arteries (parietal
lobe) and between the middle and anterior cerebral arteries (anterior frontal
lobe). If there is rapid reperfusion of the ischemic territory from lysis of the
embolic clot, blood may leak from damaged small arterioles, capillaries, and
venules, producing hemorrhagic transformation of the ischemic stroke.
Lacunar strokes are small strokes rarely greater in size than 10 mm in diameter
and are highly associated with chronic hypertension. The lesions are caused by
arteriole microvascular occlusions
Natural recovery from stroke occurs over 3 to 6 months.
In general, 70% of motor recovery occurs in the first month and 90% occurs by
3 months.
Recovery of speech is slower, with 90% recovery by 6 months.
In hemiparetic patients, 80% walk again but only 10% regain full use of the
paretic hand.
Factors associated with a good recovery include young age, mild stroke
severity, high level of consciousness, previous independence, living with a partner,
high frequency of social contacts, and positive mood.
The latter factors suggest patient motivation is important in recovery.
Introduction
Lateral medullary infarction (LMI) is the classical stroke involving the lateral
medulla (Figure 8-3) and dramatically demonstrates the multiple clinical signs
that develop when there is damage to many important tracts and nuclei.
Spinocerebellar Ataxia
Introduction
Spinocerebellar ataxias (SCAs) are a group of genetic diseases characterized by progressive loss of
coordination and balance. The incidence of SCA 1 is 1 to 2 cases per 100,000 population. Most SCAs are
autosomal–dominantly inherited.
Three pathologic mechanisms of SCA have been identified.
- The most common type (over 60% of cases) is a polyglutamine disorder resulting from proteins with toxic
stretches of polyglutamine.
- Other types are gene-expression disorders resulting from repeat expansions outside of coding regions or
channelopathies resulting from disruption of calcium or potassium channel function.
Common features of many polyglutamine SCA diseases include:
(1) onset in adulthood,
(2) slow progression,
(3) neuronal loss in the cerebellum, brainstem, and spinal cord,
(4) instability and expansion of a trinucleotide repeat tract,
(5) mutant protein aggregation or clumping in the nucleus of involved neurons, and
(6) occurrence of anticipation or the tendency for disease onset to be more severe and occur at a
younger age in the next generation.

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V LECTURE

Lecturer: Ekaterine Mamukelashvili

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