10 central nervous system disorder Patho 2 winter 2016

Terms in this set (17)

Incidence: Polio occurs primarily in children and is now rare in the western developed countries. It is still found in underdeveloped countries. In the 1930's to the early 1950's, polio was pandemic and was the largest recent epidemic with the highest mortality rate, until the advent of AIDS.

Etiology and Pathogenesis:
There are many strains of the poliovirus, only some of which cause paralysis.
The poliovirus enters the mouth and subsequently enters the digestive system,
lymphoid tissues, blood, and eventually the nervous system where it shows selective affinity. The virus is highly contagious and before vaccinations were used, produced worldwide epidemics. Eventually the virus invades the lower motor neurons of the spinal cord and brain stem.
Damage by the virus to the lower motor neurons is the primary event, exciting an
intense inflammatory reaction and loss of the anterior horn cells. There are mild cases and severe cases depending upon the extent of infection and inflammation.
Signs and Symptoms: The polio virus causes a wide range of manifestations, including nonspecific minor illness of fever, malaise, and headache, lasting 1-3 days, or else a major illness with systemic symptoms of fever, headache, muscle pain and spasm progressing to flaccid paralysis. The distribution of the paralysis varies according to which segments of the cord are
involved. Given the random distribution of affected neurons the paralysis is
asymmetrical. If the anterior horns of the phrenic nerve are damaged, respiratory failure may occur. Restoration of function may be due to neurons not being completely destroyed or
reinnervation by collateral axons sprouting from surviving neurons and forming large
motor units for that muscle.
Treatment:
Massage treatment is given after the end of the acute infection and follows the
treatment guidelines for flaccid paralysis. Massage therapy may continue during convalescence and after recovery for lasting paralysis. It is not likely that you will treat anyone who has suffered from a recent bout of acute poliomyelitis.
1. tremor at rest 2. sluggish intention of movements (poverty of movement) 3. muscle rigidity 4. postural instability
Incidence: 1 in 250 people over age 40; 1 in 100 over 65
Etiology: While the cause is idiopathic, there is a loss of the neurons in the substantia nigra of the basal ganglia and midbrain, which release dopamine.
Secondary Parkinsonism may be caused by encephalitis, trauma, carbon monoxide poisoning, and infarction in the midbrain.
Pathophysiology: The loss of dopamine leads to loss of inhibition from the basal ganglia. This loss of inhibition leads to unchecked excitation from areas that control movements.
Signs and symptoms:
1. The condition begins insidiously with a resting pill-rolling tremor of one hand. The tremor is maximal at rest, lessens with movement, and disappears while sleeping. It is enhanced by emotional tension or fatigue. The hands, arms, and legs usually are most affected, in that order. Many patients display only rigidity and never manifest tremor.
2. Reflexes and strength are often normal.
3. Hypertonia and progressive rigidity
4. Slowness and poverty of movement (bradykinesia), and difficulty in initiating movement.
5. Rigidity and hypokinesia may contribute to muscular aches and sensations of fatigue.
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6. The face has a blank expression and is mask-like (Parkinson's mask) and open- mouthed, with diminished blinking. Patient may drool, or choke.
7. Posture becomes stooped.
8. Patients find it difficult to start walking; the gait becomes shuffling with short steps, and the arms are held flexed to the waist and fail to swing with the stride. The steps may inadvertently quicken and the patient may break into a run to keep from falling. This is a festinating gait (festination).
9. A loss of balance and tendency to fall forward or backward when the center of gravity is displaced results from the loss of postural reflexes.
Note: most symptoms appear together in what is known as Parkinson's syndrome: tremor, hypertonus, rigidity, blank face, festination. [There is also loss of balance, frequent falling, and poverty of movement.]
Massage Treatment: Full body massage to try to lessen rigidity. Lots of PROM and gentle stretching Medical : Medications such as levadopa (carbidopa) which can produce side effects of
athetosis, involuntary movements of tongue and lips, head bobbing, grimacing Stem cell transplants, DBS, laser surgery
Etiology: MS is idiopathic and listed as an autoimmune disease. Incidence:
Women get MS more than men. Age of onset: 20 - 40 years.
Disease course:
MS is a slowly progressive CNS disease. Its course highly varied and unpredictable with remissions and persistently recurring exacerbations.
MS begins as scattered patches of inflammation on the white matter causing patches of demyelination and formation of scar tissue (fibrous gliosis) called plaque. Thus, degeneration of the myelin sheath occurs due to destruction of the oligodendroglia. This results in disruption of normal neuronal transmission.
There is a predilection for the lateral and posterior columns, and optic tracts.
Life span in most cases is of normal length, and the average duration of illness probably exceeds 25 years but variability is great. Some patients have frequent attacks and are rapidly incapacitated.
Signs and symptoms: Because of the scattered nature of plaque formations, there is a diversity and multiplicity of neurological signs and symptoms in both motor and sensory systems. Cognitive and limbic areas can also be affected. The disease can present with varied mental, affective, motor (somatic and autonomic), and sensory signs and symptoms.
Early in the disease course:
tingling and numbness in arms, legs, trunk, and face visual disturbances: double vision (diplopia); partial blindness weakness and clumsiness in leg or hand stiffness and fatigability of limbs minor gait disturbances vertigo difficulty with bladder control mild emotional disturbances
Late in the disease course:
mental symptoms: apathy, dementia, depression, mania, inattention. motor symptoms: hyperreflexia, tremor, spasticity, ataxia, contracture and
paralysis sensory: hypoesthesia, numbness, paraesthesia, burning and shooting pain autonomic: urinary and defecatory problems
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IMPORTANT NOTE: Excess heat may accentuate symptoms and signs.
Treatment:
Medical: Drugs; attention to stress. Psychosocial support.
Massage: Full body massage with focus on spasticity. Increase ROM of joints and address contractures and deformity if present. Watch for decubitus ulcers.
"Massage and passive movement of weakened spastic limbs make patients more comfortable." -Merck Manual
Seizures are abnormal repetitive electrical discharges in the brain. Seizures may result from:
traumatic brain injury
poisons (i.e. some venoms, or alcohol poisoning)
metabolic imbalances (hypoglycemia and hypercalcemia)
epilepsy.
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Seizures may take different forms for different people; they range from barely noticeable to life threatening.
Epilepsy is a seizure disorder caused by neurological damage that is irreversible.
Types of Seizures: Generalized Seizures - result from discharges in both cerebral hemispheres.
These are sometimes referred to as petit mal and grand mal seizures. Petit mal
seizures are characterized by brief interruptions in awareness and activity. Grand
mal or tonic-clonic seizures are characterized by contraction of muscles resulting in
violent movements of the extremities, loss of consciousness, bowel and bladder
incontinence, ending in bilateral rhythmic contraction of the limbs. Status Epilepticus - this is a medical emergency where the seizure does not stop,
or many seizures occur in rapid succession without the client regaining
consciousness.
Massage for the client with seizure disorder:
When treating a client with epilepsy, the massage therapist needs to be familiar with the type, triggers, and duration of the client's seizures. Note that massage for an epileptic client is not for their epilepsy but instead for their chief complaint or concern.
A contingency plan or protocol should be in place should the client have a seizure during the session. This needs to be established before beginning the treatment. Aura or prodromal symptoms may precede a seizure. The client and therapist should establish a hand signal or other way the client can signal the therapist should the client feel a seizure coming on.
The therapist should also take extra precautions not to trigger a seizure. Flashing lights, certain patterns on walls or fabric, odors (such as scented oils or candles), lack of sleep, and changes in body chemistry (fasting, food allergies) are all possible triggers.
The therapist should give a relaxation-based massage, avoiding abrupt movements as well as deep, vigorous, or painful techniques.
Should the client experience a seizure during the session the therapist should not attempt to restrain them or place anything in their mouths. The therapist should stay with the client and try to protect them from bumping into anything in the room.
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If the seizure lasts longer than 10 minutes or if the client gets injured during the seizure, the client should go to the hospital. However, this is the client's choice to make if they are cognizant to do so.
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