NPTE pathologies Flashcards
Amyotrophic lateral sclerosis or leu-gherigs disease
Degenerative disease seen with UMN impairments and LMN impairments. Loss of anterior horn cells in spinal cord cause weakness and muscle atrophy.
Cause: more common in men. Disease begins in all between 40-70.
Signs: UMN symptoms: ataxia, spasticity, clonus and +babinski. LMN symptoms: asymmetric muscle weakness, fasiculations, atrophy whithin hands. Weakness spreads distal to proximal path.
ALS patients will exhibit fatigue, oral motor impairment, motor paralysis and eventual respiratory failure.
Alzheimers
Neuro degenerative disorder with irreversible damage. ACH transmission inhibited within cerebral cortex. Amyloid plaques and nurofibrillary tangles forms.
Signs: change in higher cortical functions such as new learning, subtle memory changes and loss of concentration.
Treat: medications to inhibit acetylcholinesterase or cholinergic agents(SE: parasympathetic effects).
Bell palsy
Lower motor neuron disease
Temporarily unilateral facial paralysis due to trauma
Or demyelination of facial nerve.
Cause- common between 15-45 yrs of age. Can be due to 2dary effect herpes simplex/zoster virus.
Signs: assymetrical facial appearance, drooping of eyelid and mouth, dryness in eye, inability to close eyelid due to weakness and drooling
Treat: better outcome with early management. Meds: severe pts are given antiviral drugs and high dose corticosteroids.
Carpal tunnel syndrome.
(LMND) Peripheral nerve entrapment median. Sensory and motor.
Cause: Repritive use, diabetes, RA, trauma, fracture and wrist sprain, hypothyroidism.
Symptoms: night pain, weakness in hand, muscle atrophy, decrease grip strength and wrist mobility.
Treat: splinting, ergonomic measure, corticosteroid injections and PT. surgical release for severe cases.
Diabetic neuropathy
Caused by Direct effect of DM.
Cause: high blood glucose; duration of diabetes.
Symptoms: weakness and sensory disturbances occur distally. Tingling, numbness, or pain in feet. Stocking glove sensory distribution impairments, orthostatic hypotension.
Treat: strict monitoring of blood glucose, PT treats pain management, foot care and overall symptoms.
Epilepsy
Hyper synchronous electrical activity in brain. Seizure is a transient event( abrupt burst of energy) that is a symptom of interrupted brain function. One seizure alone does not signify epilepsy.
Caused: idiopathic. Increase risk with CVA, genetic, head trauma, CP, Down syndrome and autism.
Treat: antiepileptic meds. Serious side effects such as ataxia, headache and blurred vision.
Guillan barre syndrome
Lower motor neuron symptoms.
Temporary inflammation and demyelination of the peripheral nerves.
Cause: idiopathic but can be autoimmune to previous respiratory infection, flu, or immunization
Signs: motor weakness distal to proximal progression, sensory impairments and possible respiratory paralysis. Weakness progresses toward UE and head. Symptoms peak within 2-4 weeks of onset. Life threatening if respiratory involvement.
Treat: meds: requitre to be given in hospital only. Cardiac monitoring and mechanical ventilation.
PT treat pulmonary rehab strengthening, mobility training, WC and orthotic prescription and or AD training.
Huntingtons disease
Degeneration of basal ganglia and cerebral cortex.
Cause: genetic autosomal dominant trait. IT-15 gene.
Signs: common between 35-55 yrs of age. Affective dysfunction and cognitive impairment. Involuntary choreic movements, ataxia
PT: maximize endurance, strength, balance, posture and functional mobility.
MS
Demyelination of myelin sheaths around brain and spinal cord.
Cause: theory of slow acting virus causing autoimmune response. Symptoms occur at any age but commonly high between 20-35 yrs of age.
symptoms: visual problems, paresthesia and sensory changes, clumsiness, weakness, ataxia, balance dysfunction and fatigue. Intention tremor.
PT treat includes: regulation of activity level, relaxation, energy conservation technique, balance and gait training.
Myasthenia gravis:
Autoimmune disease resulting in neuromuscular junction pathology. ACH receptors blocked by antibodies preventing muscle contraction.
Cause: autoimmune. Enlarged thymus, diabetes, RA, lupus.
Cardinal signs: extreme fatiguability, skeletal muscle weakness that fluctuates within minutes or extended period of time. (Can fluctuate hour to hour). Proximal muscles more affected than distal.
Ocular mucked affected first causing ptosis and Diploplia. Dysphagia, dysarthria and CN weakness are common findings.
Treat: MG crisis is a medical emergency where exacerbation includes respiratory difficulty, swallowing issues, labored talking or chewing. Meds: anticholinesterase drugs and long term corticosteroids.
PT treat: obtain respiratory baseline, pulmonary intervention. Avoid strenuous exercise and excessive heat or cold as it exacerbates symptoms. Mod to max isometric contractions are good for strengthening. Due to steroids possible osteoporosis treatment might be required.
PD
Primary degenerative disorder. Decreased dopamine production.
Cause: genetics, carbon monoxide poisoning, other neuro degenerative disease.
Most commonly in pts aged 50-79.
Symptoms: resting tremor, difficulty with bed mobility and fine movement( writing, dressing), akinesia, festinating and shuffling gait, bradykinesia, dysphagia, cogwheel and lead pipe rigidity. Freezing.
Treatment: dopamine replacement agents( 1 hour after meds is best time for therapy)
Post-polio syndrome
Viral infection resulting in neuropathy. LMND that affects anterior horn cells.
Signs: progressive weakness, fatigue, muscle atrophy, pain and swallowing issues.
Treat: no meds for PPS
PT treats: functional indepence l, adaptive equipment, pt education.
CVA
Lack of oxygen to an area of brain 2ndary to ischemia or cell death.
Transient ischemic attack: atherosclerotic thrombosis which causes temporary interruption of blood supply to brain. Common in carotid and vertbrobasilar artery.
Completed stroke: CVA that presents complete neurological deficits at onset.
Stroke in evolution: CVA caused by thrombus that gradually progresses.
Hemorrhage: 10-15% of CVAs. Bleed in brain due to rupture. Hypertension primary cause. Presents with severe headache, vomiting, HTN and abrupt onset of symptoms.
Ischemic stroke: loss of perfusion to a portion of the brain.
Embolus: 20% of ischemic CVAs. Associated with CVD. Common site for embolus MCA from carotid arteries. Occurs rapidly with no warning and presents with headache.
Thrombus: this CVA occurs during sleep or during awakening after MI or post surgery.
