Endovascular treatment and complication prevention
One of the modern methods of surgical intervention in vascular catastrophes is endovascular aneurysm occlusion. The essence of this approach is the delivery of special thrombosing agents directly into the cavity of the affected vessel using a catheter. Most often, microcoils or platinum filaments are used as such agents. A dense blood clot (thrombus) forms around the introduced structure. It is securely fixed in the aneurysm dome, which ensures the complete cessation of pathological blood flow in this area.
To prevent severe complications, in particular rebleeding, the patient is prescribed strict bed rest lasting from three to four weeks. During this period, it is critically important to maintain stable blood pressure readings. In addition, any straining must be avoided, therefore the care regimen includes mandatory prevention of constipation, up to and including the regular use of laxatives.
To prevent the development of vasospasm and increase the resistance of nerve tissue to oxygen starvation (ischemia), calcium channel blockers are used. The drug of choice in this situation is nimodipine. In the first hours and days after a vascular catastrophe (from five to seven days), it is administered intravenously by drip at a dosage of 15–30 mcg/kg/h. Subsequently, the patient is switched to oral administration (30–60 mg up to six times a day) lasting from two to three weeks. In some cases, oral administration may be prescribed from the very beginning of therapy.
Dyscirculatory encephalopathy: causes and stages
Dyscirculatory encephalopathy (DEP) occurs against the background of the same risk factors as acute cerebrovascular accidents. The key triggers are arterial hypertension, atherosclerotic vascular disease, diabetes mellitus, and atrial fibrillation.
Depending on the severity of neurological and cognitive deficit, three stages of the disease are distinguished:
- Stage I. Characterized by mild cognitive impairments. Patients complain of memory decline, slight absent-mindedness, and reduced concentration. There is a general slowing of mental processes, as well as a decrease in the speed of motor reactions.
- Stage II. A more noticeable suppression of memory and regulatory functions occurs. It becomes objectively difficult for the patient to cope with complex intellectual tasks requiring an analytical approach.
- Stage III. Gross cognitive deficit develops. The patient completely or partially loses the ability to adapt in everyday life, society, and the professional sphere, which is classified as dementia.
Vascular dementia and its neuroimaging
Vascular dementia is most often the consequence of a series of previous strokes, both with a prominent clinical picture and "silent" ones that proceeded asymptomatically. Sometimes even a single stroke can lead to dementia if the lesion affects areas strategically important for intellect: the left frontal lobe, the thalami, or the junction area of the parietal, temporal, and occipital lobes of the left hemisphere. A mixed form is often encountered, where vascular pathology is combined with a neurodegenerative process (Alzheimer's disease).
Magnetic resonance imaging (MRI) in patients with severe (third) stage reveals a complex of specific changes:
- Significant white matter lesion — leukoaraiosis (detected in periventricular and subcortical areas).
- Pronounced cerebral tissue atrophy.
- Reduction in the thickness of cerebral gyri.
- Widening of cortical sulci.
- Hydrocephalus (pathological enlargement of the ventricular system of the brain).
Instrumental diagnostics and treatment
The diagnosis is established comprehensively. In addition to history taking (identifying transient ischemic attacks) and neuropsychological testing, instrumental methods play a huge role. CT and MRI allow the detection of traces of old strokes (glial changes, cysts), assessment of the degree of cortical atrophy and the prevalence of leukoaraiosis, the severity of which clearly correlates with the stage of encephalopathy. Ultrasound duplex scanning (UDS) is used to search for occlusions and stenoses in extracranial and intracranial arteries.
Differential diagnosis is necessarily carried out with frontotemporal dementia, brain tumors, Alzheimer's disease, chronic subdural hematomas, as well as anxiety and depressive disorders.
Principles of pharmacotherapy: Treatment is aimed at global stroke prevention. If vascular dementia has already formed, drugs similar to those used in Alzheimer's disease therapy are employed. Two main groups are used:
- Central acetylcholinesterase inhibitors: donepezil (2–4 mg per day), rivastigmine (2–6 mg per day), or galantamine (8–16 mg per day).
- Glutamate receptor blockers: memantine at a daily dosage of 10 to 20 mg.
Briefly: answers to topical questions
Which major longitudinal arterial tracts supply blood to the spinal cord?
The major longitudinal arterial tracts supplying blood to the spinal cord are the anterior and posterior spinal arteries.
- Anterior spinal artery (a. spinalis anterior) — nourishes the most significant structures of the anterior and lateral divisions (anterior horns, spinothalamic tracts, and part of the pyramidal tracts).
- Posterior spinal arteries — the main longitudinally oriented vessels descending between the posterior roots and lateral funiculi, providing blood supply to the posterior half of the spinal cord (posterior funiculi, roots, and horns).
From which segmental levels does the great anterior radiculomedullary artery of Adamkiewicz most frequently originate?
The great anterior radiculomedullary artery of Adamkiewicz (a. radicularis magna) most frequently originates at the level of the lower thoracic or upper lumbar vertebrae.
It is the largest radicular artery and serves as the main source of blood supply to the lower thoracic, lumbar, and sacral segments of the spinal cord. During ontogenesis, it elongates following the spinal cord and empties into the anterior spinal artery at an acute angle.
What clinical symptoms comprise the anterior spinal artery syndrome (Preobrazhensky syndrome)?
Anterior spinal artery syndrome presents with the sudden development of a neurological deficit accompanied by pain.
When the upper cervical region is affected, the clinical picture includes:
- Flaccid paresis of the arms due to damage to the anterior horns and roots.
- Analgesia and thermanesthesia in the upper extremities due to damage to the lateral spinothalamic pathways.
- Spastic paraparesis due to damage to the corticospinal tracts.
- Pelvic organ dysfunction — of the urinary bladder and rectum.
Epicritic and proprioceptive sensitivity are preserved because the posterior funiculi lie outside the basin of the anterior spinal artery.
What symptoms characterize posterior spinal artery syndrome (Williamson syndrome)?
Posterior spinal artery syndrome manifests as a symptom complex caused by ischemic damage to the posterior funiculi, roots, and horns of the spinal cord.
The clinical picture includes:
- Impairment of deep sensation — loss of epicritic and proprioceptive sensitivity below the level of the lesion.
- Segmental sensory disturbances — occur directly at the level of the lesion due to damage to the posterior roots.
- Spastic paraparesis — develops additionally if the corticospinal tracts are involved in the lesion focus.
Which segments of the spinal cord belong to critical zones of watershed (borderzone) blood supply?
The upper cervical and midthoracic regions belong to the critical zones of borderzone blood supply to the spinal cord.
In these zones, arterial blood flow critically depends on the anterior spinal system of adjacent vascular territories. Due to these blood supply characteristics, trauma or vascular disorders in these areas frequently lead to irreversible spinal cord injury.
What types of sensory disturbances occur with ischemia of the anterior two-thirds of the spinal cord?
Ischemia of the anterior parts of the spinal cord (in the anterior spinal artery territory) results in a dissociated type of sensory impairment.
There is a classical loss of superficial pain and temperature sensitivity (analgesia and thermoanesthesia) due to damage to the spinothalamic tracts. Meanwhile, epicritic, tactile, vibration, and proprioceptive sensitivity (joint position sense) remain intact, as the posterior columns of the spinal cord are not supplied by this artery.
Class and exam questions
What is leukoaraiosis and where is it localized?
This is a rarefaction of the cerebral white matter resulting from chronic ischemia. On tomograms, it is predominantly detected around the ventricles (periventricularly) and beneath the cerebral cortex (subcortically).
Which brain regions are considered "strategic" for the development of dementia following a single stroke?
Such zones include the thalami, the frontal lobe of the left hemisphere, and the junction area of the parietal, temporal, and occipital lobes of the left hemisphere.
What dosages of memantine are used in vascular dementia?
Memantine, a glutamate receptor blocker, is prescribed at a daily dosage of 10 to 20 mg.
What else to study on this topic
- Mechanisms of periventricular leukoaraiosis development
- Neuropsychological testing in various stages of dyscirculatory encephalopathy
- Mixed dementia: criteria for the combination of vascular factors and Alzheimer's disease
- Dosing principles of acetylcholinesterase inhibitors in clinical practice
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