Stroke: Introduction

Essentials of Diagnosis

Sudden onset of characteristic neurologic deficit. Patient often has history of hypertension, diabetes mellitus, valvular heart disease, or atherosclerosis. Distinctive neurologic signs reflect the region of the brain involved.

Table 24–4. Features of the major stroke subtypes.Stroke Type and Subtype

Clinical Features Diagnosis Treatment

Ischemic strokeLacunar infarct Small (< 5 mm) lesions in the basal

ganglia, pons, cerebellum, or internal capsule; less often in deep cerebral white matter; prognosis generally good; clinical features depend on location, but may worsen over first 24–36 hours.

CT may reveal small hypodensity but is often normal.

Aspirin; long-term management is to control risk factors (hypertension and diabetes mellitus).

Carotid circulation obstruction

See text—signs vary depending on occluded vessel.

Noncontrast CT to exclude hemorrhage; CT may be normal during first 6–24 hours of an ischemic stroke, whereas diffusion-weighted MRI is more sensitive; electrocardiography, blood glucose, complete blood count, and tests for hypercoagulable states, hyperlipidemia are indicated; echocardiography or Holter monitoring in selected instances.

Select patients for intravenous thrombolytics or intra-arterial mechanical thrombolysis; aspirin (325 mg/d orally) combined with sustained-release dipyridamole (200 mg twice daily) is first-line therapy; anticoagulation with heparin for cardioembolic strokes, and sometimes for evolving stroke when no contraindications exist.

Vertebrobasilar occlusion

See text—signs vary based on location of occluded vessel

As for carotid circulation obstruction As for carotid circulation obstruction

Hemorrhagic strokeSpontaneous intracerebral hemorrhage

Commonly associated with hypertension; also with bleeding disorders, amyloid angiopathy.

Noncontrast CT is superior to MRI for detecting bleeds of < 48 hours duration; laboratory tests to identify bleeding disorder: angiography may be indicated to exclude aneurysm or AVM. Do not perform lumbar puncture.

Most managed supportively, but cerebellar bleeds or hematomas with gross mass effect benefit from urgent surgical evacuation.

Location: basal ganglia more

common than pons, thalamus, cerebellum, or cerebral white matter.

Subarachnoid hemorrhage

Present with sudden onset of worst headache of life, may lead rapidly to loss of consciousness; signs of meningeal irritation often present; etiology usually aneurysm or AVM, but 20% have no source identified.

CT to confirm diagnosis, but may be normal in rare instances; if CT negative and suspicion high, perform lumbar puncture to look for red blood cells or xanthochromia; angiography to determine source of bleed in candidates for treatment.

See sections on AVM and aneurysm.

Intracranial aneurysm

Most located in the anterior circle of Willis and are typically asymptomatic until subarachnoid bleed occurs; 20% rebleed in first 2 weeks.

CT indicates subarachnoid hemorrhage, and angiography then demonstrates aneurysms; angiography may not reveal aneurysm if vasospasm present.

Prevent further bleeding by clipping aneurysm or coil embolization; nimodipine helps prevent vasospasm; reverse vasospasm by intravenous fluids and induced hypertension after aneurysm has been obliterated, if no other aneurysms are present; angioplasty may also reverse symptomatic vasospasm.

AVMs Focal deficit from hematoma or AVM itself.

CT reveals bleed, and may reveal the AVM; may be seen by MRI. Angiography demonstrates feeding vessels and vascular anatomy.

Surgery indicated if AVM has bled or to prevent further progression of neurologic deficit; other modalities to treat nonoperable AVMs are available at specialized centers.

Primary Intracranial Tumors

Essentials of Diagnosis

Generalized or focal disturbance of cerebral function, or both. Increased intracranial pressure in some patients. Neuroradiologic evidence of space-occupying lesion.

Table 24–5. Primary intracranial tumors.Tumor Clinical Features Treatment and PrognosisGlioblastoma multiforme

Presents commonly with nonspecific complaints and increased intracranial pressure. As it grows, focal deficits develop.

Course is rapidly progressive, with poor prognosis. Total surgical removal is usually not possible. Radiation therapy and chemotherapy may prolong

survival.Astrocytoma Presentation similar to glioblastoma multiforme but course more protracted,

often over several years. Cerebellar astrocytoma may have a more benign course.

Prognosis is variable. By the time of diagnosis, total excision is usually impossible; tumor may be radiosensitive and chemotherapy may also be helpful. In cerebellar astrocytoma, total surgical removal is often possible.

Medulloblastoma Seen most frequently in children. Generally arises from roof of fourth ventricle and leads to increased intracranial pressure accompanied by brainstem and cerebellar signs. May seed subarachnoid space.

Treatment consists of surgery combined with radiation therapy and chemotherapy.

Ependymoma Glioma arising from the ependyma of a ventricle, especially the fourth ventricle; leads to early signs of increased intracranial pressure. Arises also from central canal of cord.

Tumor is best treated surgically if possible. Radiation therapy may be used for residual tumor.

Oligodendroglioma Slow-growing. Usually arises in cerebral hemisphere in adults. Calcification may be visible on skull x-ray.

Treatment is surgical and usually successful. Radiation and chemotherapy may be used if tumor has malignant features.

Brainstem glioma Presents during childhood with cranial nerve palsies and then with long tract signs in the limbs. Signs of increased intracranial pressure occur late.

Tumor is inoperable; treatment is by irradiation and shunt for increased intracranial pressure.

Cerebellar hemangioblastoma

Presents with disequilibrium, ataxia of trunk or limbs, and signs of increased intracranial pressure. Sometimes familial. May be associated with retinal and spinal vascular lesions, polycythemia, and renal cell carcinoma.

Treatment is surgical. Radiation is used for residual tumor.

Pineal tumor Presents with increased intracranial pressure, sometimes associated with impaired upward gaze (Parinaud's syndrome) and other deficits indicative of midbrain lesion.

Ventricular decompression by shunting is followed by surgical approach to tumor; irradiation is indicated if tumor is malignant. Prognosis depends on histopathologic findings and extent of tumor.

Craniopharyngioma Originates from remnants of Rathke's pouch above the sella, depressing the optic chiasm. May present at any age but usually in childhood, with endocrine dysfunction and bitemporal field defects.

Treatment is surgical, but total removal may not be possible. Radiation may be used for residual tumor.

Acoustic neurinoma Ipsilateral hearing loss is most common initial symptom. Subsequent symptoms may include tinnitus, headache, vertigo, facial weakness or numbness, and long tract signs. (May be familial and bilateral when related to neurofibromatosis.) Most sensitive screening tests are MRI and brainstem auditory evoked potential.

Treatment is excision by translabyrinthine surgery, craniectomy, or a combined approach. Outcome is usually good.

Meningioma Originates from the dura mater or arachnoid; compresses rather than invades adjacent neural structures. Increasingly common with advancing age. Tumor

Treatment is surgical. Tumor may recur if removal is incomplete.

size varies greatly. Symptoms vary with tumor site—eg, unilateral proptosis (sphenoidal ridge); anosmia and optic nerve compression (olfactory groove). Tumor is usually benign and readily detected by CT scanning; may lead to calcification and bone erosion visible on plain x-rays of skull.

Primary cerebral lymphoma

Associated with AIDS and other immunodeficient states. Presentation may be with focal deficits or with disturbances of cognition and consciousness. May be indistinguishable from cerebral toxoplasmosis.

Treatment is high-dose methotrexate followed by radiation therapy. Prognosis depends on CD4 count at diagnosis.

Head Injury

Table 24–7. Acute cerebral sequelae of head injury.Sequelae Clinical Features PathologyConcussion Transient loss of consciousness with bradycardia, hypotension, and respiratory arrest

for a few seconds followed by retrograde and posttraumatic amnesia. Occasionally followed by transient neurologic deficit.

Bruising on side of impact (coup injury) or contralaterally (contrecoup injury).

Cerebral contusion or laceration

Loss of consciousness longer than with concussion. May lead to death or severe residual neurologic deficit.

Cerebral contusion, edema, hemorrhage, and necrosis. May have subarachnoid bleeding.

Acute epidural hemorrhage

Headache, confusion, somnolence, seizures, and focal deficits occur several hours after injury and lead to coma, respiratory depression, and death unless treated by surgical evacuation.

Tear in meningeal artery, vein, or dural sinus, leading to hematoma visible on CT scan.

Acute subdural hemorrhage

Similar to epidural hemorrhage, but interval before onset of symptoms is longer. Treatment is by surgical evacuation.

Hematoma from tear in veins from cortex to superior sagittal sinus or from cerebral laceration, visible on CT scan.

Cerebral hemorrhage

Generally develops immediately after injury. Clinically resembles hypertensive hemorrhage. Surgical evacuation is sometimes helpful.

Hematoma, visible on CT scan.

Hipoglikemia

HypoglycemiaWhen the blood glucose falls around 54 mg/dL, the patient starts to experience both sympathetic (tachycardia, palpitations, sweating, tremulousness) and parasympathetic (nausea, hunger) nervous system symptoms. If these autonomic symptoms are ignored and the glucose levels fall further (around 50 mg/dL), then neuroglycopenic symptoms appear, including irritability, confusion, blurred vision, tiredness, headache, and difficulty speaking. A further decline in glucose can then lead to loss of consciousness or even a seizure. With repeated episodes of hypoglycemia, there is adaptation, and autonomic symptoms do not occur until the blood glucose levels are much lower and so the first symptoms are often due to neuroglycopenia. This condition is referred to as "hypoglycemic unawareness." It has been shown that hypoglycemic unawareness can be reversed by keeping glucose levels high for a period of several weeks. Except for

sweating, most of the sympathetic symptoms of hypoglycemia are blunted in patients receiving -blocking agents for angina pectoris or hypertension.

Though not absolutely contraindicated, these drugs must be used with caution in insulin-requiring diabetics, and 1-selective blocking agents are preferred.

Hypoglycemia in insulin-treated patients with diabetes occurs as a consequence of three factors: behavioral issues, impaired counterregulatory systems, and complications of diabetes.

Behavioral issues include injecting too much insulin for the amount of carbohydrates ingested. Drinking alcohol in excess, especially on an empty stomach, can also cause hypoglycemia. In patients with type 1 diabetes, hypoglycemia can occur during or even several hours after exercise, and so glucose levels need to be monitored and food and insulin adjusted. Some patients do not like their glucose levels to be high, and they treat every high glucose level aggressively. These individuals who "stack" their insulin—that is, give another dose of insulin before the first injection has had its full action—can develop hypoglycemia.

Counterregulatory issues resulting in hypoglycemia include impaired glucagon response, sympatho-adrenal responses, and cortisol deficiency. Patients with diabetes of greater than 5 years duration lose their glucagon response to hypoglycemia. As a result, they are at a significant disadvantage in protecting themselves against falling glucose levels. Once the glucagon response is lost, their sympatho-adrenal responses take on added importance. Unfortunately, aging, autonomic neuropathy, or hypoglycemic unawareness due to repeated low glucose levels further blunts the sympatho-adrenal responses. Occasionally, Addison's disease develops in persons with type 1 diabetes mellitus; when this happens, insulin requirements fall significantly, and unless insulin dose is reduced, recurrent hypoglycemia will develop.

Complications of diabetes that increase the risk for hypoglycemia include autonomic neuropathy, gastroparesis, and renal failure. The sympathetic nervous system is an important system alerting the individual that the glucose level is falling by causing symptoms of tachycardia, palpitations, sweating, and tremulousness. Failure of the sympatho-adrenal responses increases the risk of hypoglycemia. In addition, in patients with gastroparesis, if insulin is given before a meal, the peak of insulin action may occur before the food is absorbed causing the glucose levels to fall. Finally, in renal failure, hypoglycemia can occur presumably because of decreased insulin clearance as well as loss of renal contribution to gluconeogenesis in the postabsorptive state.

To prevent and treat insulin-induced hypoglycemia, the diabetic patient should carry glucose tablets or juice at all times. For most episodes, ingestion of 15 grams of carbohydrate is sufficient to reverse the hypoglycemia. The patient should be instructed to check the blood glucose in 15 minutes and treat again if the

glucose level is still low. A parenteral glucagon emergency kit (1 mg) should be provided to every diabetic receiving insulin therapy, and family or friends should be instructed how to inject it intramuscularly in the event that the patient is unconscious or refuses food.

If more severe hypoglycemia has produced unconsciousness or stupor, the treatment is 50 mL of 50% glucose solution by rapid intravenous infusion. If intravenous therapy is not available, 1 mg of glucagon injected intramuscularly will usually restore the patient to consciousness within 15 minutes to permit ingestion of sugar. If the patient is stuporous and glucagon is not available, small amounts of honey or syrup or glucose gel (15 g) can be inserted within the buccal pouch, but, in general, oral feeding is contraindicated in unconscious patients. Rectal administration of syrup or honey (30 mL per 500 mL of warm water) has been effective.