Division of Natural Sciences
Lewis-Clark State College
Chp. 16: CONCEPTS OF NEUROLOGIC DYSFUNCTION
I. Alzheimer disease
 |
cause unknown |
|
increased neuron loss |
|
characterized by two pathologies: |
|
NFT: neurofibrillary tangles in cerebral cortex and hippocampus (role in memory) |
|
neurtic plaque: axons coalesce around an amyloid core. Amyloid is a pathological protein. |
|
Clinical manifestations include:
| ||||||||
|
Treatments include new drugs like Cognex and Exelon which inhibit acetylcholine degradation and appear to improve memory. |
II. Seizures
A. Conditions associated with seizure disorders
B. Types of seizure disorders
|
Generalized: Grand mal and petit mal; both involve the RAS (reticular activating system).
| ||||
|
Partial or focal: seizure activity is limited to a discreet area of the brain. |
|
Status Epelipticus: multiple seizures without recovery between. |
C. Pathophysiology
|
seizure activity begins in epileptogenic focus. | ||||||||
|
spreads to:
|
|
Inhibitory neurons fire; intermittent contract-relax pattern of muscles |
|
Neuronal fatigue occurs
|
D. Clinical manifestations
1. petit mal
2. grand mal
|
Prodromal period : malaise, depression, headache |
|
Aura : distinctive sensation immediately before a seizure; auditory, gustatory, visual perception or a feeling of dizziness. |
|
Tonic phase : loss of consciousness, increased muscle tone, muscles contract, pt falls to floor, apnea, cyanosis, urination, defecation; last less than 1 min., usually 15 sec. |
|
Clonic phase: violent, rhythmic muscular contraction, hyperventilation, excessive salivation, profuse sweating, rapid heart rate. |
|
postictal period: pt remains in a stupor or coma for approximately 5 min. |
5. treatment
III. Parkinson Disease
A. Structure and function of the basal ganglia (see link also)
B. Pathophysiology
C. Clinical manifestations
a. rigidity - both protagonist and antagonist muscles remain tightly contracted throughout a movement. First symptoms may be muscle cramps in toes or hands.
b. tremor - usually the first symptom to appear; disappears during voluntary movement; other motor cortex and cerebellar signals override the abnormal basal ganglia signals.
c. akinesia - inability to initiate movement and decreased associated movements; all skeletal muscles are eventually affected; extremities, trunk, facial, ocular. To perform event the simplest movement, pt must exert the highest degree of concentration. This results in slowness of movement (bradykinesia). When pt. begins to perform a discrete, voluntary movement with the hands, automatic, associated adjustments to not occur (hypokinesia). Freezing may occur which may be precipitated by an increased effort to either move or turn. Pt. has a mask-like expression - no automatic, emotional facial expressions.
d. postural abnormalities - 
Ø disorders of postural fixation : involuntary flexion of the head and neck; pt unable to maintain an upright trunk position while walking/standing.
Ø disorders of equilibrium : inability to make appropriate postural adjustments to tilting or falling.
Ø disorders of righting : inability to right themselves when changing from reclining or crouching position to a stand.
e. autonomic and neuroendocrine symptoms: inappropriate diaphoresis, orthostatic hypotension, constipation, urinary retention.
D. treatment
|
Levodopa: crosses the blood brain barrier and is converted to dopamine by the enzyme dopa decarboxylase. |
|
Carbidopa: does not cross the blood brain barrier and a peripheral dopa decarboxylase inhibitor |
Chp. 17: ALTERATIONS OF NEUROLOGIC FUNCTION (not covered on DVD's; C d'A students are not responsible for this information)
A. Multiple sclerosis
1. pathophysiology
2. Clinical manifestations
a. Mixed (general) type:
Lesions in optic nerve, brain stem, and cerebellum.
Optic signs: optic neuritis
Brain stem signs: involves cranial nerves III through 12;
|
nystagamus- tremor of eyeballs |
|
intranuclear ophthalmoplegia - weakness of ocular muscles (medial rectus); failure of adduction of contralateral eye when observing an object laterally; also double vision, eye pain. |
|
dysarthria - speech that is almost unintelligible; lack of coordination of mouth, respiratory system and larynx. |
b. spinal type:
Location of lesions: corticospinal tracts and dorsal column.
Function: Corticospinal tract transmits impulses from cerebral cortex. Impulses reach skeletal muscles that coordinate precise, discreet movements. Dorsal column transmits impulses from sensory receptors. These sensations include: 2 pt discrimination, proprioception, stereognosis (the ability to recognize size and shape), weight discrimination, and vibration.
With M.S. the most common neurologic finding is spastic paraparesis (weakness in lower limbs). Also bladder and bowel dysfunction: incontinence, constipation. Tingling, numbness, and deficits in those sensations associated with the dorsal column.
c. Cerebellar Type :
Location of lesions : cerebellum (usually symmetrical)
Function: coordination and balance
Major symptoms:
Ø motor ataxia - lack of coordination; movements that can either overshoot or undershoot their mark.
Ø hypotonia - decreased tone of peripheral musculature; loss of resistance to passive movement.
Ø asthenia - muscle weakness
d. Amaurotic Form :
Location of lesions : cerebrum, optic nerve
Major symptoms:
Ø optic neuritis - impaired vision (blurry, foggy, decreased acuity) impaired color perception
3. evaluation
