i bc27f85be50b71b1 (95 page)

NERVOUS SYSTEM

3 1 3

Hemorrhagic CVA involves cerebral hypoperfusion, which is

abrupt in onset and is secondary to intra parenchymal hemorrhage

associated with hypertension, AVM, trauma, aneurysm, or SAH.

The management of hemorrhagic CVA involves blood pressure

control (low to normal range), trearment of causarive factors (if

possible), corticosteroids, anricoagulation (for reperfusion), prophylactic anticonvulsant therapy, and surgical hematoma evacuarion (if appropriate).

Experimental rrearment oprions for CVA include cytoprotective

drugs and gene transfer rherapy.3' The signs and symptoms of CVA

depend on the location (anterior vs. posterior and cortical vs. subcortical) and the extent of the cerebral ischemia or infarction. General signs and symptoms include contralateral motor and sensory loss,

speech and perceptual deficits, altered vision, abnormal muscle tone,

headache, nausea, vomiting, and altered effect.

Other terms commonly used to describe CVA include the following:

Completed stroke. A CVA in which the neurologic impairments have

fully evolved

Stroke-ill-evolutioll. A CVA in which the neurologic impairments continue to evolve or fluctuate over hours or daysJ8

LaCllllar stroke. A cerebral infarct of deep white matter (less than 1 .5

cm in diameter) due to the thrombosis of very small penetrating

cerebral vessels39

Watershed stroke. A cerebral infarcr berween the terminal areas of

perfusion of two different arteries, typically between the anterior

and middle cerebral arteries 14

Arteriovenous Malformation

AVM is a malformarion in which blood from the arterial system is

shunted to the venous system (thereby bypassing the capillaries)

through abnormally thin and dilated vessels. An AVM can occur in

a variety of locations, shapes, and sizes. The resulr of rhe bypass of

blood is degeneration of brain parenchyma around the site of the

AVM, which creates a chronic ischemic state. Signs and symptoms

of AVM include headache, dizziness, fainting, seizute, aphasia,

bruit, and motor and sensory deficits J4 Management of AVM

includes cerebral angiogram to evaluate the precise location of the

3 1 4 AClJTE CARE HANDBOOK FOR PHYSICAL THERAPISTS

AVM, followed by surgical AVM repair, embolization, radiosurgery (stereotactic), or photon beam therapy. 14

Cerebral Aneurysm

Cerebral aneurysm is the dilation of a cerebral blood vessel wall

owing to a smooth muscle defect through which the endothelial layer

penetrates. Cerebral aneurysms most commonly occur at arterial

bifurcations and in the larger vessels of the anterior circulation. Signs

and symptoms of unruptured cerebral aneurysm are determined by

size and location, such asJ4

Anterior communicating artery-Visual field deficits, endocrine dysfunction, fronral headache

Middle cerebral arrery-Aphasia, focal arm weakness, paresthesias

Basilar bifurcation-Oculomotor paresis

Signs and symptoms of ruptured aneurysm include violent headache,

stiff neck, phorophobia, vomiting, hemiplegia, aphasia, seizure, and

CN (III, IV, VI) palsy.'4 Management of cerebral aneurysm involves

CT scan or angiogram to closely evaluate the aneurysm, followed by

aneurysm clipping, embolization, or balloon occlusion.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH), the accumulation of blood in the

subarachnoid space, is most commonly the result of aneurysm rupture,

or less commonly a complication of AVM, rumor, infection, or trauma.

It is graded ftom I to V according to the Hunt and Hess scalel4;

I.

Asymptomatic

II.

Moderate to severe headache, nuchal rigidity, without

neurologic deficit

111.

Drowsiness, confusion, with mild focal neurologic deficit

IV.

Stu POt, moderate to severe focal deficits, such as hemiplegia

V.

Comatose, abnormal posturing

SAH is diagnosed by history, clinical examination, CT scan, LP, or

angiogram. The management of SAH depends on its severity and may

NERVOUS SYSTEM 315

include surgical aneurysm repair with blood evacuation; ventriculostomy; and supportive measures to maximize neurologic, cardiac, and respiratory status, rehydration, and fluid-electrolyte balance.

Complications of SAH include rebleeding, hydrocephalus, seizure,

and vasospasm. Vasospasm is the spasm (constriction) of one or more

cerebral arteries that occurs 4-1 2 days after SAH.4o Diagnosed by

either transcranial Doppler, cerebral angiography or CT, the exact etiology of vasospasm is unknown. Vasospasm results in cerebral ischemia distal to the area of spasm if untreated. The signs and symptoms of vasospasm are worsening level of consciousness, agitation, decreased strength, altered speech, pupil changes, headache, and vomiting, and they may wax and wane with the degree of vasospasm.

Vasospasm is treated with induced hypertension, hypervolemia, and

hemodilution.4o

Ventricular Dysfunction

Hydrocephalus

Hydrocephalus is the acute or gradual accumulation of CSF, causing

excessive ventricular dilation and increased JCP. CSF permeates

through the ventricular walls into brain tissue secondary to a pressure

gradient. There are twO rypes of hydrocephalus:

I .

Noncommtlllicatillg (obstrucrive) hydrocephalus, in which there

is an obstruction of CSF flow within the ventricular system. There may be

thickening of the arachnoid villi or an increased amount or viscosity of

CSF. This condition may be congenital or acquired, often as the result of

aqueduct stenosis, tumor obstruction, abscess, or cyst, or as a complication of neurosurgery.4

2.

Communicating hydrocephalus, in which there is an obstruc-

tion in CSF flow as it interfaces wirh the subarachnoid space. This

condition can occur with meningitis, after head injury, with SAH, or

as a complication of neurosurgery.2

Hydrocephalus may be of acure onset characterized by headache,

altered consciousness, decreased upward gaze, and papilledema.s

Management includes treatment of the causative factor if possible, or

ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt.

3 1 6 AClJfE CARE HANDBOOK FOR PHYSICAL THERAPISTS

Normal-pressure hydrocephalus (NPH) is a type of comminucating hydrocephalus without an associated rise in ICP and occurs primarily in rhe elderly." It is diagnosed by history, head CT, and, possibly, LP. The hallmark triad of the signs of NPH is altered mental status (confusion), altered gait, and urinary incontinence. NPH is typically gradual and idiopathic but may be associated with previous meningitis, trauma, or SAH.8 Management of NPH is typically with a VP shunt.

Cerebrospinal Fluid Leak

A CSF leak is the abnormal discharge of CSF from a scalp wound,

the nose (rhinorrhea), or rhe ear (otorrhea) as a result of a

meningeal tear. A CSF leak can occur with anterior fossa or

perrous skull fractures or, less commonly, as a complication of

neurosurgery. With a CSF leak, the patient becomes at risk for

meningitis with the altered integrity of the dura. A CSF leak,

which usually resolves spontaneously in 7-1 0 days,14 is diagnosed

by clinical history, CT cisternography, and testing of fluid from the

leak site. If the fluid is CSF (and nOt another fluid, e.g., mucus), it

will test positive for glucose. The patient may also complain of a

salty taste in the mouth. Management of CSF leak includes prophylactic antibiotics (controversial), lumbar drainage for leaks persisting more than 4 days, dural repair for leaks persisting more

than 1 0 days, or VP or VA shunt."

Clinical Tip

If it is known that a patient has a CSF leak, the therapist

should be aware of vital sign or position restrictions before

physical therapy intervention. If a CSF leak increases or a

new leak occurs during physical therapy intervention, the

therapist should stop the treatment, loosely cover the leaking area, and notify the nurse immediately.

Seizure

A seizure is a phenomenon of excessive cerebral cortex activity with

or without loss of consciousness. The signs and symptoms of the seizure depend on the seizure locus on the cortex (e.g., visual hallucina-