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AClITE CARE HANDBOOK FOR I)HYSICAL THERAPISTS

Guillain-Barre Syndrome

Guillain-Barre syndrome (GBS), or acute inflammatory demyelinating polyradiculopathy, is caused by the breakdown of Schwann cells by antibodies." There is an onset of paresthesia, pain (especially of

the lumbar spine), symmetric weakness (commonly proximal followed by distal, including the facial and respiratory musculature), and autonomic dysfunction approximately 1-3 weeks afrer a viral

infection. GBS is diagnosed by history, clinical presentation, CSF

sampling (increased protein level), and EMG studies (which show

decreased motor and sensory velocities).' Once diagnosed, the

patient with GBS is hospitalized because of the potential for rapid

respirarory muscle paralysis.4S Functional recovery varies from full

independence to residual weakness that takes J 2-24 months to

resolve." GBS is fatal in 5% of cases.'s The management of GBS

may consist of pharmacologic therapy (immunosuppressive agents),

plasma exchange, intravenous immunoglobulin, respiratory support, physical therapy, and the supportive treatmenr of associated symptoms (e.g., pain management).

Multiple Sclerosis

MS is the demyelination of the white maner of the CNS and of the

optic nerve, presumably an autoimmune reaccion. MS is categorized

by onset and progression as relapsing-remitting (clearly defined

relapses with full recovery or with residual deficit), primary progressive (occasional plateaus in disease progression and only temporary improvements), secondary progressive (initial relapsing-remitting followed by disease progression with or without relapses or plateaus), or progressive relapsing (progressive from onset with acute relapses,

with or without full recovery) J4

MS typically occurs in 20- to 40-year-olds and in women more

than men. It is diagnosed by history (the onset of symptoms must

occur and resolve more than once), clinical presentation, CSF sampling (increased myelin protein and immunoglobulin G levels), and by M R I (which shows the presence of two or more plaques of the

CNS).' These plaques are located at areas of demyelination where

lymphocytic and plasma infiltration and gliosis have occurred. Signs

and symptoms of the early stages of MS may include focal weakness, fatigue, diplopia, blurred vision, equilibrium loss (vertigo), and urinary incontinence. Additional signs and symptoms of the larrer

stages of MS may include ataxia, paresthesias, spasticity, sensory

deficits, hyper-reflexia, tremor, and nysragmus.44 The management

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of MS may include pharmacologic therapy (corticosteroids), skeletal

muscle relaxants, physical therapy, and the treatment of associated

disease manifestations (e.g., bladder dysfunction).

Parkinson's Disease

Parkinson 's disease (PO) is the idiopathic progressive onset of

bradykinesia, altered posture and postural reflexes, resting tremor,

and cogwheel rigidity. Other signs and symptoms may include shuffling gait characterized by the inability to start or stop, blank facial expression, drooling, decreased speech volume, an inability to perform fine motor tasks, and dementia." PO is diagnosed by history, clinical presentation, and MRI (which shows a light rather than

dark substantia nigra).8 The management of PO mainly includes

pharmacologic therapy with anti parkinsonian agents and physical

therapy. Stereotactic thalamotomy and the placement of a highfrequency thalamic stimulator are surgical options for symptoms refractory to medical therapy."

General Management

11.tracrallial and Cerebral Perfusion Pressure

The maintenance of normal [CP or the prompt recognition of elevated [CP is one of the primary goals of the team caring for the postcraniosurgical patient or the patient with cerebral trauma, neoplasm, or infection.

ICP is the pressure CSF exerts within the ventricles. This pressure

(normally 4- 1 5 mm Hg) fluctuates with any systemic condition, body

position, or activity that increases cerebral blood flow, blood pressure, or intrathoracic or abdominal pressure or that decreases venous return or increases cerebral metabolism.

The three dynamic variables within the fixed skull are blood, CSF,

and brain tissue. As [CP rises, these variables change in an attempt to

lower [CP via the following mechanisms: cerebral vasoconstriction,

compression of venous sinuses, decreased CSF production, or shift of

CSF to the subarachnoid space. When these compensations fail, compression of brain structures occurs, and fatal brain herniation will develop if untreated (Figure 4-8). The signs and symptoms of

increased [CP are listed in Table 4-20. The methods of controlling

Iep, based on clinical neurologic examination and diagnostic tests, are