Neuro Pathologies Flashcards
Alzheimer’s Disease
- progressive neurological disorder results in deterioration and irreversible damage in the cerebral cortex and subcortical areas of the brain
- neurons that are normally involved with acetylcholine transmission deteriorate within the cerebral cortex of the brain.
- more common in women and incidence increases over the age of 80
- changes in higher cortical functions characterized by subtle changes in memory, impaired concentration, and difficulty with new learning.
- can’t be confirmed until postmortem biopsy to confirm neurofibrillary tangles and amyloid plaques.
- meds Tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon)
What is the leading cause of death from someone with Alzheimer’s Disease?
Dehydration and infection
Stages of Alzheimer’s Disease
- Early stage: loss of orientation, word finding difficulties, emotional lability, depression, poor judgement, and impaired ability to perform self-care skills
- Middle stage: behavioral and motor problems such as aphasia, apraxia, perseveration, agitation, and violent or socially unacceptable behavior including wondering
- End-stage: ability to learn is lost and long-term memory disappears. Severe intellectual and physical destruction. Incontinence, functional dependence, and inability to speak, and seizure acitivity
Amyotrophic Lateral Sclerosis (ALS)
- chronic degenerative disease
- upper and lower motor neuron impairments
- etiology unknown. higher incidence in men. 40-70 y/o
- LMN: asymmetric m weakness, fasciculations, cramping, and atrophy in hands.
- weakness distal to proximal
- UMN: incoordination of movement, spasticity, clonus, and positive Babinski reflex
- will exhibit fatigue, oral motor impairment, motor paralysis, and eventual respiratory paralysis.
- to confirm diagnosis: EMG or m biopsy
- Riluzole (Rilutek) to help slow disease process.
- anticholinergic, antispasticity, and antidepressant
- PT focus on QOL among other things
- most likely to die due to decline in respiratory function due to infection or inability to eat. (Death is ~2-5 yr after onset)
- muscle wasting (amyotrophy) and gliotic hardening (sclerosis) of the anteiror and lateral corticospinal tracts involving UMN and LMN (pg. 160 patho book)
Typical progression of ALS from earliest to latest onset (main ones)
- fasciculations
- loss of dexterity
- dysarthria
- respiratory failure
Anterior Cord Syndrome
- Incomplete spinal cord lesion which impacts the anterior spinal artery.
*anterior spinal artery supplies blood to the anterior 2/3 of the SC
- Typically from cervical flexion injury
- Affects that anterior and lateral corticospinal tracts and spinothalamic tracts…..so…
- complete loss of motor function and loss of pain and temperature.
Arthrogryposis Multiplex Congenita (AMC)
- non-progressive neuromuscular disease that occurs during the first trimester in utero
*Etiology is unknown
- Cylinder like extremities with minimal definition, significant and multiple contractures, dislocation of joints, and m atrophy
- Treatment: to attain maximum level of development through – positioning, stretching, strengthening, splinting, and use of adaptive equipment.
Which intervention(s) would MOST likely be the initial focus of physical therapy for arthrogryposis?
Stretching and splinting
Stretching to achieve full range of motion at a contracted joint followed by splinting to maintain the acquired range of motion are the primary intervention strategies for children with arthrogryposis.
Afterwards focus on functional mobility
Arthrogryposis is usually diagnosed at birth when an infant has contractures in two or more body areas. Common areas include the foot, hip, wrist, knee, elbow, and shoulder. There is usually prenatal damage to the anterior horn cells with a decreased number of motor units. Fibrotic tissue limits normal joint development and promotes the development of contractures.
Bell’s Palsy
- acute onset of sensory and motor deficits to the area of the facial nerve due to abnormal pressure on the facial nerve from inflammation/edema
- Typically from herpes simplex/herpes zoster
*15-45 yr of age.
*Asymmetrical facial appearance with “drooping” of eyelid and mouth, potential for drooling, dryness of eyes, and inability to close the eyelid due to weakness.
- anti-viral medication, high-dose corticosteroids
- massage, stretching, and moist heat, biofeedback and NMES
*Some typically resolve in few weeks (mild) but may take up to 6 months
Carpal Tunnel Syndrome
*peripheral nerve entrapment of the median nerve under the transverse carpal ligament
- Flexor digitorum profundus tendons, four flexor digitorum superficialis tendons, and flexor pollicis longus tendon go through here.
- 35-55 yr; greater in women
- Risk factors: repetitive use, RA, pregnancy, DM, trauma, tumor, hypothyroidism, and wrist sprain or fracture
- sensory and paresthesia along median nerve distribution.
*night pain, weakness of hand, m atrophy, decreased grip strength, clumsiness, decreased wrist mobility
*Ape hand caused by atrophy of thenar musculature and first 2 lumbricals. (abductor pollicis brevis)
- Treatment - corticosteroids injections, splinting, and PT (splinting, mobilization, and gentle stretching)
- without sx - 4-6 weeks. With sx 6-8 weeks.
Central Cord Syndrome
- incomplete spinal cord lesion caused by cervical hyperextension injury typically that causes bleeding into the central gray matter
- other contributing factors: cervical spondylosis, narrowing or congenital defect of spinal canal, tumor, RA or syringomyelia
- over 50 y/o and in men
- motor loss UE>LE. Most severe distally in UE.
- Sacral segments are usually unaffected since they are located laterally within the SC
- Methylprednisolone should be administered within 8 hrs of injury to assist with neurological recovery.
- CCS is the most common incomplete spinal cord lesion.
Cerebral Palsy
- umbrella term for brain damage occured in utero that is non-progressive.
*Etiology -of oxygen, maternal infections, drug or alcohol abuse, placents abnormalities, toxemia, prolonged labor, prematurity, and p incompatibility. The etiology of acquired cerebral palsy include meningitis, CVA, seizures, and brain injury.
- Signs and symptoms - demonstrate abnormal muscle tone, impaired modulation of movement, presence of abnormal reflexes, and impaired mobility. (Range from mild to severe)
2 types of cerebral palsy primary motor patterns
*Spastic - indicating a lesion in the motor cortex of the cerebrum; upper motor neuron damage
* Athetoid - indicating a lesion involving the basal ganglia
Distribution of involvement of Cerebral palsy motor patterns
- Monoplegia - one extremity
- Diplegia - bilateral lower extremity involvement, howevel. upper extremities may be affected
- Hemiplegia - unilateral involvement of the upper and loved extremities
Quadriplegia - involvement of the entire body
CVA Risk Factors
- Primary: HTN, cardiac disease or arrhythmias, DM, cigarette smoking, TIA
- Secondary: Obesity, high cholesterol, behavior related to HTN (stress, increase salt intake), physical inactivity, increased alcohol consumption.
*Modifiable: HTN, atherosclerosis, heart disease, DM, elevated cholesterol, smoking, and obesity
HTN is the most prevalent modifiable cause.
- Non-modifiable: age, race, family hx, and sex.
Age is the greatest risk for CVA (>65 y/o)
What will you see with a L CVA vs R CVA?
L CVA:
- weakness/paralysis on R side
- impaired processing
(difficulty processing communication and processing information in a sequential, linear manner, difficulty with verbal commands)
- heighted frustration
- aphasia
- dysphagia
- motor apraxia
- R hemianopsia
- decreased discrimination b/n L&R
R CVA:
- weakness/paralysis on L side
- poor attention span
- impaired awareness and judgement
- spatial deficits
- memory deficits
- L inattention (neglect)
- decreased abstract reasoning
- emotional lability
- impulsive behavior
- L hemianopsia
Most common artery for CVA?
middle
What will you see if a stroke in the brainstem vs cerebellum?
Brainstem:
- unstable vital signs
- Decreased consciousness
- decreased ability to swallow
- weakness/paralysis on BOTH sides of the body
Cerebellum:
- decreased balance
- ataxia
- decreased coordination
- nausea
- decreased ability for adjustment
- nystagmus
Diabetic Neuropathy
- direct effect of DM
- nerve ischemia from direct effects of hyperglycemia (from prolonged exposure to high blood glucose).
- weakness and sensory disturbances distally in symmetrically.
- tingling, numbness or pain (especially of the feet)
- wasting of muscles of the feet or hands “stocking glove” sensory distribution impairment, orthostatic hypotension, weakness, urinary impairments, and significant pain.
Down Syndrome
AKA trisomy 21
* Incomplete cell division of the 21st pair of chromosomes. …this results in 47 chromosomes. (Normal odd 46)
- Advanced maternal age increases the risk of the genetic imbalance
- S&S: intellectual disability, hypotonia, joint hypermobility, developmental delay, flattened nasal bridge, narrow eyelids with epicanthal folds, small mouth, feeding impairment, flat feet, scoliosis, congenital heart disease, and visual and hearing loss.
- PT will not accelerate developmental milestones…it will help avoid compensatory patterns with static positions and mobility
- Exercise is essential for child with Down syndrome in order to avoid inactivity and obesity
Duchenne Muscular Dystrophy
- progressive disorder – absence of gene needed for muscle proteins dystrophin and nebulin. mutation of dystrophin Xp21
- cell membranes weaken, myofibrils are destroyed, and m contractility is lost.
- Fat and connective tissue replace muscle
- Death typically from cardiopulmonary failure before age 25
- X-linked recessive gene…so the mother is a silent carrier. And only men get it
- usually diagnosed around 2-5 y/o
- waddling gait, progressive weakness, disinterest in running, falling, toe walking, excessive lordosis, and pseudohypertrophy of m. , difficulty with stair climbing
*Gowers sign
*is this the one you don’t over work them and you get them a chair sooner rather than later?
- typically loose ability to ambulate around 10-12 y/o
- 1/3 have learning disability
Erb’s Palsy
- upper brachial plexus injury/palsy
- Typically from difficulty deliver (breech position, prolonged labor, large baby, use of forceps) the neck gets stretched and damages the nerves
- Affects C5-6: axillary, lateral pectoral, upper and lower subscapular, suprascapular, and partial paralysis of the long thoracic and musculocutaneous nerves
- Loose the rotator cuff, deltoid, brachialis, coracobrachialis, and biceps brachii functions.
- “Waiter’s tip position”: loss of shld function, loss of elbow flexion, loss of forearm supination, and hand positioned in pinch grip.
- PT: work on active and passive movement that promotes the use of the weak UE for functional activities.
- Spontaneous recovery can occur in 3-4 mths. If conservative fails – surgery then splint for 3-4 weeks.
Epilepsy
- temporary dysfunction of the brain
- Conditions that increase risk: genetic influence, head trauma, dementia, CVA, cerebral palsy, DS, and autism
- S&S: mood disturbances, staring, LOC, uncontrollable jerking of the arms and legs, stiffening of the muscles, and loss of m control.
- EMG measures the electrical activity of the brain….most common test used to confirm the diagnosis.
- one seizure doesn’t signal epilepsy
Guillain-Barre Syndrome
- temporary inflammation and demyelination of the peripheral nerves myelin sheath. (aka acute polyneuropathy)
- most common in the young adult pts and again in 5th-8th decades
- Etiology: autoimmune response to previous respiratory infection, influenza, immunization, or sx. OR viral infections, Epstein-Barr syndrome, SMV, or bacterial infections
- S&S: (rapidly ascending symmetric motor weakness and distal sensory impairments)
- motor weakness distal to proximal (distal symmetrical motor impairment)
- sensory impairment
- transient paresthesia’s that progresses towards the UE and head.
- first sign typically paresthesia’s in the toes
- peaks at 2-4 weeks; but recovery can last from 3-12 months
- can have life threatening respiratory impairment
- diagnosed through CSF ( high protein levels and little to no lymphocytes). EMG will have abnormal and slowed conduction
- Acute: PROM, positioning, and light exercise. Limit overexertion and fatigue to avoid exacerbation of symptoms.
- majority of pts experience full recover, 20% have remaining neurologic deficits, and 3-5% of pts die from respiratory complications.
After 1 yr 67% have complete recovery, while 20% have significant disability. At 2 yrs 8% still have not recovered.