Binswanger's disease

The subcortical arteriosclerotic encephalopathy ( SAE, Synonyms: Binswanger disease, vascular encephalopathy ) is a by vascular changes (atherosclerosis ) caused disease of the brain ( encephalon ), which leads beneath the cerebral cortex (cortex ) that is to subcortical damage ( pathology ). It was first described by the Swiss psychiatrist Otto Ludwig Binswanger (1852-1929) in Jena.

Pathogenesis

The SAE (ie, a decrease in the nerve cell fibers that connect the cerebral cortex with the subcortical brain structures ) characterized by many infarcts in combination with a vascular demyelination of the Mark camp with diffuse density reduction around the brain ventricles ( periventricular ) in a CT image. This ischemia seem to be only by changes in the vessel wall ( lipohyalinosis ) caused less lying in the deeper brain arteries. This leads to a thickening of the vessel wall, which leads to a narrowing of the lumen. Demyelination appears to be caused by ischemia, which is caused by the decrease in the perfusion pressure in hypotensive episodes. In patients with SAE often be arterial hypertension, diabetes mellitus and recurrent infarctions found in different brain regions.

A similar pathological- anatomical picture show progressive multifocal leukoencephalopathy, leukodystrophy and mitochondrial diseases

Symptoms

It can be summarized characteristic symptoms hardly, since the small infarcts not necessarily be symptomatic. However, primarily the medulla is concerned, it can be assumed that mainly occur in disorders of impulse conduction. Often, but not necessarily, and often after several years, there may occur an intellectual and affective flattening ( " leveling " ) in combination with neuropsychological disorders.

In late-onset subcortical arteriosclerotic encephalopathy can lead to a subcortical vascular dementia, this is probably for most of the symptoms of vascular dementia (co) responsible. Characteristic symptoms of subcortical arteriosclerotic encephalopathy are:

It is a legs - insecure, clumsy gait, which is usually described as " frontal " or " DYSPRAXIC ", but does not imitate the small steps - rhythmic " shuffling " of Parkinson's disease. Muscle tone is spastic increases, so the pyramidal tract involved in the symptomatology. The emphasis on the lower extremities corresponding to the position of the tracks, the topographical arrangement shows the trajectories for the legs most medial ( ventrikelnahe ). The tendon reflexes are increased ( in Parkinson's disease weakened or absent ) and the pyramidal signs often positive.

Urgency and leakage of urine to the urinary incontinence are common, the central bubble train connects directly to the orbits of the legs laterally.

Slowdown and loss of drive similar to the behavior in Parkinson's disease, and the social withdrawal is an early symptom. Subsequently, paranoid- hallucinatory symptoms happen while the noopsychischen cortical functions such as abstract thinking and long-term memory for a long time remain unaffected. The dementia progresses but continued.

  • Restriction of the higher brain functions ( dementia ) and
  • Two of the following symptoms High pressure or general vascular disease
  • Chronic vascular insufficiency
  • Subcortical dysfunction ( gait disturbance, rigidity, bladder disorder )

The behavioral disturbances in dementia patients are called BPSD ( Behavioural and Psychological Symptoms of Dementia ). Below you count the apathy ( 76.0 %), Aberrant motor behavior ( = aimless wandering ) ( 64.5 %), eating disorders ( eating Unessbarem ) ( 63.7 %), irritability / lability ( 63.0 %), agitation / aggression ( 62.8 %), insomnia ( 53.8 % ), depression / dysphoria ( 54.3 % ), anxiety ( 50.2 %), delusions ( 49.5 %), disinhibition ( 29.5% ), hallucinations ( 27.8 %), and euphoria ( 16.6 %).

Diagnostic Imaging

The diagnosis is confirmed with an MRI (magnetic resonance imaging = magnetic resonance imaging ). This shows in the T2 - weighted images, typical whitish confluent foci around the ventricles and especially on the front and rear ends of the lateral ventricles a cap-like sclerosis zone. The differential diagnosis to distinguish them is the "Status lacunaris " multi- infarction cause a similar clinical picture especially in patients with atrial fibrillation, in the same areas where small infarcts ( mini-strokes ).

Therapy

A causal therapy exists to date not because the exact cause of the SAE is not released. There is no surgical treatment options. The possibilities of influencing drug are low. The therapeutic goal should be both short-term as well as longer-term hypotonic hypertonic episodes to avoid, as this combination is a considerable risk factor SAE.

Physiotherapy

Because of the emphasis put on extrapyramidal movement disorder that area first comes to the most important. New strategies to compensate for the imbalance, the gait disturbance and the disturbance of coordination are necessary and must be started early.

Occupational Therapy

Because of the disturbance of coordination, especially the two-hand coordination and the combination with apraxia symptoms, their use is important. Continence advice and the gift of adequate resources, supply of incontinence material and advice about the drinking habits make life easier for patients and their relatives.

Cognitive training

Used by psychologists and occupational therapists or even performed together and aims at independence, responsibility and better orientation. In behavioral recently non-pharmacological interventions are favored. Only if this is not sufficient, will be resorted to medical aid.

Differential Diagnosis

  • Normal pressure
  • Alzheimer's disease
  • Multiple sclerosis
  • Leukodystrophy
  • Cerebral edema
  • HIV encephalopathy
  • Progressive multifocal leukoencephalopathy
Otto Binswanger Recidivism (medicine) Clinical neuropsychology Parkinson's disease Psychomotor agitation Major depressive disorder
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