8 NERVOUS SYSTEM
TYPE OF CVA DESCRIPTION Ischemic:
Thrombotic
Most common cause of CVA
Frequently the result of atherosclerosis; also associated with hypertension, smoking, diabetes Thrombus in extracranial or intracranial vessel blocks blood flow to the cerebral cortex
Carotid artery most commonly affected extracranial vessel
Common intracranial sites include bifurcation of carotid arteries, distal intracranial portion of vertebral arteries, and proximal basilar arteries
May occur during sleep or shortly after awakening; during surgery; or after a myocardial infarction
Ischemic: Embolic Second most common type of CVA
Embolus from heart or extracranial arteries floats into cerebral bloodstream and lodges in middle cerebral artery or branches
Embolus commonly originates during atrial fibrillation Typically occurs during activity
Develops rapidly
Ischemic: Lacunar Subtype of thrombotic CVA
Hypertension creates cavities deep in white matter of the brain, affecting the internal capsule, basal ganglia, thalamus, and pons
Lipid coating lining of the small penetrating arteries thickens and weakens wall, causing microaneurysms and dissections
Hemorrhagic Third most common type of CVA
Typically caused by hypertension or rupture of aneurysm
Diminished blood supply to area supplied by ruptured arteriy and compression by accumulated blood
Initially, the ruptured cerebral blood vessels may constrict to limit the blood loss. This vasospasm further compromises blood flow, leading to more ischemia and cellular damage. If a clot forms in the vessel, decreased blood flow also promotes ischemia. If the blood enters the subarachnoid space, meningeal irritation occurs. The blood cells that pass through the vessel wall into the surrounding tissue also may break down and block the arachnoid villi, causing
hydrocephalus.
Signs and symptoms
The clinical features of CVA vary according to the affected artery and the region of the brain it supplies, the severity of
the damage, and the extent of collateral circulation developed. A CVA in one hemisphere causes signs and symptoms on the opposite side of the body; a CVA that damages cranial nerves affects structures on the same side as the infarction.
General symptoms of a CVA include:
unilateral limb weakness speech difficulties
numbness on one side headache
visual disturbances (diplopia, hemianopsia, ptosis) dizziness
anxiety
altered level of consciousness.
Additionally, symptoms are usually classified by the artery affected. Signs and symptoms associated with middle cerebral artery involvement include:
aphasia dysphasia
visual field deficits
hemiparesis of affected side (more severe in face and arm than leg).
Symptoms associated with carotid artery involvement include:
weakness paralysis numbness
sensory changes
visual disturbances on the affected side altered level of consciousness
bruits headaches aphasia ptosis.
UNDERSTANDING TIAs
A transient ischemic attack (TIA) is an episode of neurologic deficit resulting from cerebral ischemia. The recurrent attacks may last from seconds to hours and clear within 12 to 24 hours. It is usually considered a warning sign for cerebrovascular accident (CVA). In fact, TIAs have been reported in over one-half of the patients who have developed a CVA, usually within 2 to 5 years.
In a TIA, microemboli released from a thrombus may temporarily interrupt blood flow, especially in the small distal branches of the brain's arterial tree. Small spasms in those arterioles may impair blood flow and also precede a TIA.
The most distinctive features of TIAs are transient focal deficits with complete return of function. The deficits usually involve some degree of motor or sensory dysfunction. They may range to loss of consciousness and loss of motor or sensory function, only for a brief time. Commonly the patient experiences weakness in the lower part of the face and arms, hands, fingers, and legs on the side opposite the affected region. Other manifestations may include transient dysphagia, numbness or tingling of the face and lips, double vision, slurred speech, and dizziness.
Symptoms associated with vertebrobasilary artery involvement include:
weakness on the affected side numbness around lips and mouth visual field deficits
diplopia
poor coordination dysphagia
slurred speech dizziness nystagmus amnesia ataxia.
Signs and symptoms associated with anterior cerebral artery involvement include:
confusion weakness
numbness, especially in the legs on the affected side incontinence
loss of coordination
impaired motor and sensory functions
personality changes.
Signs and symptoms associated with posterior cerebral artery involvement include:
visual field deficits (homonymous hemianopsia) sensory impairment
dyslexia
preservation (abnormally persistent replies to questions) coma
cortical blindness
absence of paralysis (usually).
Complications
Complications vary with the severity and type of CVA, but may include:
unstable blood pressure (from loss of vasomotor control) cerebral edema
fluid imbalances sensory impairment
infections, such as pneumonia altered level of consciousness aspiration
contractures
pulmonary embolism death.
Diagnosis
Computed tomography identifies ischemic stroke within first 72 hours of symptom onset, and evidence of hemorrhagic stroke (lesions larger than 1 cm) immediately.
Magnetic resonance imaging assists in identifying areas of ischemia or infarction and cerebral swelling.
Cerebral angiography reveals disruption or displacement of the cerebral circulation by occlusion, such as stenosis or acute thrombus, or hemorrhage.
Digital subtraction angiography shows evidence of occlusion of cerebral vessels, lesions, or vascular abnormalities.
Carotid duplex scan identifies stenosis greater than 60%.
Brain scan shows ischemic areas but may not be conclusive for up to 2 weeks after CVA.
Single photon emission computed tomography (SPECT) and positron emission tomography (PET) identifies areas of altered metabolism surrounding lesions not yet able to be detected by other diagnostic tests.
Transesophageal echocardiogram reveals cardiac disorders, such as atrial thrombi, atrial septal defect or patent foramen ovale, as causes of thrombotic CVA.
Lumbar puncture reveals bloody CSF when CVA is hemorrhagic.
Ophthalmoscopy may identify signs of hypertension and atherosclerotic changes in retinal arteries.
Electroencephalogram helps identify damaged areas of the brain.
Treatment
Treatment is supportive to minimize and prevent further cerebral damage. Measures include:
ICP management with monitoring, hyperventilation (to decrease partial pressure of arterial CO2 to lower ICP), osmotic diuretics (mannitol, to reduce cerebral edema), and corticosteroids (dexamethasone, to reduce
inflammation and cerebral edema)
stool softeners to prevent straining, which increases ICP anticonvulsants to treat or prevent seizures
surgery for large cerebellar infarction to remove infarcted tissue and decompress remaining live tissue aneurysm repair to prevent further hemorrhage
percutaneous transluminal angioplasty or stent insertion to open occluded vessels.
For ischemic CVA:
thrombolytic therapy (tPa, alteplase [Activase]) within the first 3 hours after onset of symptoms to dissolve the clot, remove occlusion, and restore blood flow, thus minimizing cerebral damage (See Treating ischemic CVA.)
anticoagulant therapy (heparin, warfarin) to maintain vessel patency and prevent further clot formation.
For TIAs:
antiplatelet agents (aspirin, ticlopidine) to reduce the risk of platelet aggregation and subsequent clot formation (for patients with TIAs)
carotid endarterectomy (for TIA) to open partially occluded carotid arteries.
For hemorrhagic CVAs:
analgesics such as acetaminophen to relieve headache associated with hemorrhagic CVA.
Guillain-Barré syndrome
Also known as infectious polyneuritis, Landry-Guillain-Barré syndrome, or acute idiopathic polyneuritis, Guillain-Barré syndrome is an acute, rapidly progressive, and potentially fatal form of polyneuritis that causes muscle weakness and mild distal sensory loss.
This syndrome can occur at any age but is most common between ages 30 and 50. It affects both sexes equally.
Recovery is spontaneous and complete in about 95% of patients, although mild motor or reflex deficits may persist in the feet and legs. The prognosis is best when symptoms clear before 15 to 20 days after onset.
This syndrome occurs in three phases:
Acute phase begins with onset of the first definitive symptom and ends 1 to 3 weeks later. Further deterioration does not occur after the acute phase.
Plateau phase lasts several days to 2 weeks.
Recovery phase is believed to coincide with remyelinization and regrowth of axonal processes. It extends over 4 to 6 months, but may last up to 2 to 3 years if the disease was severe.
Causes
The precise cause of Guillain-Barré syndrome is unknown, but it may be a cell-mediated immune response to a virus.
About 50% of patients with Guillain-Barré syndrome have a recent history of minor febrile illness, usually an upper respiratory tract infection or, less often, gastroenteritis. When infection precedes the onset of Guillain-Barré syndrome, signs of infection subside before neurologic features appear.
Other possible precipitating factors include:
surgery
rabies or swine influenza vaccination Hodgkin's or other malignant disease systemic lupus erythematosus.
Pathophysiology
The major pathologic manifestation is segmental demyelination of the peripheral nerves. This prevents normal
transmission of electrical impulses along the sensorimotor nerve roots. Because this syndrome causes inflammation and degenerative changes in both the posterior (sensory) and the anterior (motor) nerve roots, signs of sensory and motor losses occur simultaneously. (See Understanding sensorimotor nerve degeneration.) Additionally, autonomic nerve transmission may be impaired.
Signs and symptoms
Symptoms are progressive and include:
symmetrical muscle weakness (major neurologic sign) appearing in the legs first (ascending type) and then extending to the arms and facial nerves within 24 to 72 hours, from impaired anterior nerve root transmission muscle weakness developing in the arms first (descending type), or in the arms and legs simultaneously, from impaired anterior nerve root transmission
muscle weakness absent or affecting only the cranial nerves (in mild forms)
paresthesia, sometimes preceding muscle weakness but vanishing quickly, from impairment of the dorsal nerve root transmission
diplegia, possibly with ophthalmoplegia (ocular paralysis), from impaired motor nerve root transmission and involvement of cranial nerves III, IV, and VI
dysphagia or dysarthria and, less often, weakness of the muscles supplied by cranial nerve XI (spinal accessory nerve)
hypotonia and areflexia from interruption of the reflex arc.