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
Clinical Features Diagnosis Treatment
Ischemic stroke
Lacunar 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
Aspirin; long-term management is to control risk
factors (hypertension and diabetes mellitus).
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
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.
See text—signs vary based on
location of occluded vessel
As for carotid circulation obstruction As for carotid circulation obstruction
Hemorrhagic stroke
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
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
perform lumbar puncture.
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.
Most located in the anterior circle of
Willis and are typically
asymptomatic until subarachnoid
bleed occurs; 20% rebleed in first 2
CT indicates subarachnoid hemorrhage, and
angiography then demonstrates aneurysms;
angiography may not reveal aneurysm if vasospasm
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 Prognosis
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
Astrocytoma Presentation similar to glioblastoma multiforme but course more protracted,
often over several years. Cerebellar astrocytoma may have a more benign
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
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.
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
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
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.
Treatment is surgical. Tumor may recur if removal is
Primary cerebral
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

Head Injury
Table 24–7. Acute cerebral sequelae of head injury.
Sequelae Clinical Features Pathology
Concussion 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
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
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.
Generally develops immediately after injury. Clinically resembles hypertensive
hemorrhage. Surgical evacuation is sometimes helpful.
Hematoma, visible on CT scan.

When 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
-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.