Acute Neurological Deficit

Acute Neurological Deficit

1. DEFINITION

   • Decrease in the functioning of the brain, spinal cord, muscles, or nerves and is defined as the presence of one or more of the following signs:
     • Acute impairment of mental function (memory loss), language disorder
     • Acute onset of paralysis (<2 weeks)
     • Decreased sensitivity, Loss of balance
     • Involuntary movements
     • dysfunction of the neurological system.

2. EPIDEMIOLOGY

   • Stroke is the 2do leading cause of death worldwide, with 6.2 million dying from stroke in 2015, an increase of 830,000 since the year 2000.

3. ETIOLOGY

   • Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds.
   • If the cessation of flow lasts for more than a fewminutes, infarction or death of brain tissue results.
   • When blood flow is quickly restored, this is called a transient ischemic attack.
   • the neurologic signs and symptoms last for >24 h or brain infarction is demonstrated.
   • Intracranial hemorrhage the toxic effects of blood itself, or by increasing intracranial pressure.

4. PATHOPHYSIOLOGY

   • ISCHEMIC STROKE
     • Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies.
     • A decrease in cerebral blood flow to zero causes death of the brain tissue within 4-10 minutes.
     • Tissue surrounding the core region of infraction is ischemic but reversibly dysfunctional and is referred to as the ischemic penumbra.
     • Focal cerebral infarction occurs via two distinct pathways:
       • A necrotic pathway
       • An apoptotic pathway
     • Ischemia produces necrosis by starving neurons of glucose and oxygen, which in turn results in failure of mitochondria to produce ATP.
       • Without ATP, membrane ion pumps stop functioning and neurons depolarize, allowing intracellular calcium to rise.
   • INTRACRANEAL HEMORRHAGE
     • Hypertensive intraparenchymal hemorrhage usually results from spontaneous rupture of a small penetrating artery deep in the brain.
     • The hemorrhage may be small or a large clot may form and compress adjacent tissue, causing herniation and death.
     • Blood may dissect into the ventricular space, which substantially increases morbidity and may cause hydrocephalus.

5. CLASSIFICATION

   • Ischemic stroke or cerebral infarction:
     • it occurs because there is an obstruction of an artery , and it can be classified as follows:
       • Atherothrombotic
       • Cardioembolic
       • Lacunar infarction
       • Unusual infarction
       • Indeterminate
   • Hemorrhagic stroke:
     • It is caused by the rupture of a blood vessel in the brain causing hemorrhage, it is classified as follows:
       • Cerebral or parenchymal hemorrhage
       • Subarachnoid Hemorrhage

6. CLINICAL MANIFESTATIONS

   • The clinical manifestations presented by the patient depend on the exact part of the brain that is affected
   • Symptoms of stroke :
     • Facial drooping
     • Arm weakness
     • Speech difficulties
     • Time

7. DIAGNOSIS

   • The gold standard for stroke diagnosis are imaging studies for example:
     • CT scans
       • CT radiographic images identify or exclude hemorrhage as the cause of stroke, and they identify extraparenchymal hemorrhages
     • MRI
       • MRI reliably documents the extent and location of infarction in all areas of the brain, including the posterior fossa and cortical surface.
       • It also identifies intracranial hemorrhage and other abnormalities but is less sensitive than CT for detecting acute blood.
     • Cerebral angiography
       • Conventional x-ray cerebral angiography is the gold standard for identifying and quantifying atherosclerotic stenoses of the cerebral arteries and for identifying other pathologies,
     • Ultrasound techniques

8. TREATMENT

   • The gold of ischemic stroke treatment is to preserve the ischemic penumbra.
   • Interfering with platelet aggregation is the best-studied pharmacological intervention in secondary prevention of CVA.
     • Acetylsalicylic acid
       • causes a non-reversible inhibition of the enzyme cyclooxygenase, responsible for preventing platelets from adhering to the endothelium,
       • 324 mg of ASA is recommended for secondary prevention of CVA.
     • Ticlopidine
       • 250 mg twice daily
     • Clopidogrel
       • It works by inhibiting ADP-induced platelet aggregation.