Subcortical arteriosclerotic encephalopathy

Subcortical arteriosclerotic encephalopathy

Description, Causes and Risk Factors:

Subcortical arteriosclerotic encephalopathy disease is a sometimes dementing illness for which chronic arterial hypertension has been implicated as a major pathogenetic factor. It had been considered to be rare, but recent reports suggest that it is fairly common. Illustrations of CT images in this disorder have been restricted almost exclusively to severe cases. The CT appearance of the advanced cases, specifically excessive periventricular radiolucency, is well known, but lesser degrees of involvement are less well appreciated.

There are numerous risk factors underlying these changes, such as age, hypertension, hypotension, smoking, inadequate diet, and diabetes mellitus. A number of genetic factors may also play a role. Hyperhomocysteinemia and hyperlipidemia have been identified daytime hypertension, hypertensive crises, and the absence of a normal nocturnal dip in blood pressure are considered to be particularly damaging. Another factor that may play a role in the development of progression of subcortical arteriosclerotic encephalopathy is coagulation activation leading to a hypercoagulable state.

The relationship between systemic arterial hypertension and subcortical arteriosclerotic encephalopathy is not clear. Hypertension might be the sole etiologic factor, a necessary but not the only causative agent, or a contributing but non-requisite element.

    60 patients with clinical and computed tomographic (CT) features of subcortical arteriosclerotic encephalopathy were reviewed. It is concluded that the features were sufficiently characteristic for subcortical arteriosclerotic encephalopathy to be considered as a sub-category of cerebrovascular disease and an identifiable cause of dementia in the elderly. Sixteen patients in this series underwent radioisotope brain scintiscan, in which the dynamic radionuclide scintiangiography (RSA) correlated with the clinical course. An increased mean plateau/peak value in the hemispheric curves is seen in the deteriorating patients in contrast to the stable patients.

  • The abnormality of gait that may occur in patients with subcortical arteriosclerotic encephalopathy is described in 12 patients in whom difficulty walking was the presenting symptom. Their gaits had elements of both Parkinsonism and ataxia, which were most marked in 4 patients unable to stand unaided. The difficulty in using their legs to walk was out of proportion to that of other movements of the lower limbs when lying or seated. In contrast, upper limb mobility and facial expression were relatively preserved. Attention is drawn to the similarity of this gait pattern to that of some patients with hydrocephalus, frontal lobe lesions, and "senile" disorders of gait. A possible mechanism for this Parkinsonian-ataxia in these various conditions may be their propensity to damage the afferent and efferent interconnections of the leg areas of the motor and supplementary motor areas of the cerebral cortex with, the cerebellum and basal ganglia.

  • Eleven patients with subcortical arteriosclerotic encephalopathy were assessed psychometrically, and the results compared with control subjects without neurological disorders and patients with a single cerebrovascular lesion. The groups were matched for sex, age, years of education, the nature, site and size of the discrete vascular lesion. The subcortical arteriosclerotic encephalopathy patients had mild-to-moderate impairment in intellectual, memory, receptive language and constructional functions, but individual performance ranged from near normality to severe impairment. The differences between the performance of subcortical arteriosclerotic encephalopathy patients and the controls were significant in the majority of tests. The subcortical arteriosclerotic encephalopathy patients had lower scores than cerebrovascular lesion patients on all tests, but in many of these the difference was not significant.

The age of onset is between 40 to 60 years and most patients have a history of chronic hypertension often poorly controlled and often one or more vascular incidents.


There are several different signs and symptoms to watch for that may be an indication of this ailment. Some of these are:

    An inability to act or make decisions.

  • Changes in personality or mood.

  • Difficulty with walking.

  • A lack of facial expression.

  • Depression.

  • The loss of bladder control (urinary incontinence).

  • Problems with speech.

  • Short-term memory loss.

  • Forgetfulness.

  • Apathy or indifference.

  • Slowness of conduct.

  • Irritability.

  • Clumsiness.


There are no specific laboratory markers for the disease. In uncomplicated cases of subcortical arteriosclerotic encephalopathy, CT and MRI identify a relatively well preserved cortex moderately to more seriously enlarged ventricles and a board area of reduced density around the ventricles on CT or MRI, a zone of high signal intensity on T2-weighted and FLAIR images involving the periventricular and deep white matter.


There is no cure for subcortical arteriosclerotic encephalopathy. Whenever hypertension is present, treating it may slow down the progress of disease. Other risk factors such as hyperlipidemia and hyperhomocysteinemia should be treated. There is some evidence that in an early stage the disease can still be influenced by these measures. Some success has been booked with medications. The robust evidence for the effectiveness of cholinergic treatments in Alzheimer's disease, and the frequent occurrence of mixed dementias, has led to the testing of galantamine in a group of patients with subcortical arteriosclerotic encephalopathy. Galantamine has a dual cholinergic mode of action, and reduces behavioral symptoms in Alzheimer's disease. This is the result of its potential-to-modulate systems involving other neurotransmitters such as serotonin and dopamine, which affect mood and emotional balance. Application of galantamine in subcortical arteriosclerotic encephalopathy patients led to significant cognitive improvement over 6 months, long-term maintenance of cognition for at least 12 months and improvement of both behavioral and functional symptoms.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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