Nerve and Muscle Flashcards by Sam James

Any Disorder of the peripheral nervous system involving either the axon or the myelin sheath

 May be localized or generalized

nerve and muscle

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toxic substance

lead neuropathy

steroid neuropathy

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demyelinating disease

Guillain Barre Syndrome

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Axonopathies

Crohn’s Disease

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Demyelinating/ axonal loss

Diabetes Mellitus neuropathies

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tells the 3 types of destruction of the nerve

SEDDON’S CLESSIFICATION

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often times can recover, normally it would present as conduction block

Neuropraxia

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axon are severed

Axonotmesis

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totally no connection anymore

Neurotmesis

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this classification is very important in surgery because the nerve transection repair should be approximated properly depending on the level of severity

SUNDERLAND’S CLASSIFICATION

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neuropraxia)

 Focal conduction block

FirstDegree

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Axonotmesis)

 Concentric needle

 Axonal damage and wallerian degeneration with intact supporting structures

Second degree injury

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Neurotmesis)

 Interruption of axon and endoneurium

Third Degree Injury

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Interruption of perineurium and endoneurium

Fourth Degree Injury

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Complete cut

Fifth degree injury

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often times the mainstay in dx, b/c some conditions are demyelinating.

It evaluates the integrity of the nerve and muscle

Electrodiagnosis

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Nerve Conduction study, Somatosensory evoke potentials,

Nerve conduction study (NCS)

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Divided into 2: electromyography and single fiber testing

Electromyography

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nerve usually have faster response b/c of saltatory conduction

myelinated

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slower b/c they don’t have the myelin sheath and nodes of ranvier.

unmyelinated

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Will require you to have electrodes and stimulators.

 Electrodes are placed in a certain area and you will find where it will pass through.

Nerve conduction study (NCS)

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needle that has 2 needles inside.

 Has one major outer needle, which is usually positive

 Third Degree Injury (Neurotmesis)

 Interruption of axon and endoneurium

and the reference, and the much inner needle which is the active and is negative.

 It can pick up a very huge number of signals

Concentric needle

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one polar needle, which is usually positive.

 Fifth degree injury

 Complete cut

 The active electrode which is usually negative is the one incorporated with the monopolar needle.

Monopolar needle

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Antidromic (studies are performed by recording potentials directed toward the sensory receptors)

Non-Physiologic response

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will stimulate a portion and placed the recording electrode near the proximal portion, which is called as orthodromic testing. (Studies are obtained by recording potentials directed away from these receptors.

physiologic response

Sensory Nerve Action potential  Smaller signal, 10 microvolts  More sensitive

SNAP

Compound Motor Action Potential  Signal is bigger because it has 2 mv

CMAP

It will tell amplitude, latency and duration.

CMAP

tells us how far or how fast that signal came to u from point A to point B.

Conduction velocity

Primary sensory peripheral neuropathy (acroneuropathy)  Antidromic (studies are performed by recording potentials directed toward the sensory receptors) o Autonomic Peripheral Neuropathy o Acute painful Neuropathy o Subclinical Neuropathy  SNAP  Sensory Nerve Action potential  Smaller signal, 10 microvolts  More sensitive o Proximal lower extremity motor neuropathy (diabetic amyotrophy)

Symmetrical | Diabetic neuropathy

Neuropathy of individual nerves (mononeuropathy) o Some Painful Neuropathy o Truncal Neuropathy or radiculopathy o Entrapment Neuropathy

Asymmetrical DN

Rare  Severe pain in the distal lower extremities  Associated with weight loss, depressionand insomnia  Mild sensory loss  Inappropriately labeled “neuritis”

Acute Painful Neuropathy

Sensory loss and: o Orthostatic hypotension o Gastrointestinal dysautonomia o Esophageal dysmotility o Gastroparesis Diarrhea or Constipation neurogenic bladder erectile dysfunction impaired distal sweating

Autonomic Peripheral Neuropathy

Initially thought of as a “spinal cord lesion”  Earlier called “diabetic amyotrophy”  Electrodiagnostically noted as a dysfunction in the proximal peripheral nerve  May be acute or subacute  Weakness of quads, iliopsoas, or thigh adductors or in combination  May also include gluteal muscles, hamstrings and gastrocnemius  Pain (Severe, Deep and aching)  Sensory is usually intact Recovery occurs over a 12 to 24 month period  Prognosis for recovery is good

Lower Extremity Proximal Motor Neuropathy

Seen in older patients (50 and above)  May be acute or gradual  Unilateral distribution  Usually T3 through T12

Truncal Neuropathy or Radiculopathy

Studies suggest by Frasier et al that there is no clear cut relationship between this neuropathies and diabetes

Entrapment Neuropathy

Also known as Acute Demyelinating Polyradiculopathy (AIDP)  An acquired symmetrical polyneuropathy  Affects the lower extremity first  Etiology: unknown  May be due to a viral insult on the myelin and schwann cell IDIOPATHICBRACHIAL NEURITIS  Onset: 1 to 4 wks post illness, vaccination or surgery  Males affected more than females

GUILLAIN-BARRÉ SYNDROME

Ascending sensory abnormalities  Ascending symmetrical weakness  Possibly bedridden in two days  CN VII most affected  CN I and II not affected  Respiratory or autonomic failure

GUILLAIN-BARRÉ SYNDROME

GUILLAIN-BARRÉ SYNDROME | ancillary

CSF  increased protein, few mononuclear cells  EMG

GUILLAIN-BARRÉ SYNDROME | tx

Plasmapharesis  IV immunoglobulins  Respiratory support  Steroids usually not effective

GUILLAIN-BARRÉ SYNDROME | rehab aims

Maintain Muscle bulk and range of motion  Splinting to prevent Contractures  Orthotics and assistive devices  Improve endurance

HEREDITARY MOTOR SENSORY NEUROPATHY I)

CHARCOT MARIE TOOTH DISEASE

Most frequently inherited neurologic disease Prevalence rate: 125,000 in US Chromosome 17 Autosomal Dominant Age onset: Early childhood (1st to 2nd decade of life)

CHARCOT MARIE TOOTH DISEASE

Progressive  Abnormal Vibration and proprioception  Abnormal muscle stretch response  Foot intrinsic atrophy  Pes Cavus -Hammer Toes  Bilateral foot drop  Stork leg appearance  Hypertrophy of peripheral nerves  Greater auricular nerve

CHARCOT MARIE TOOTH DISEASE

CHARCOT MARIE TOOTH DISEASE ancillary

CSF tap-increased protein  Onion bulb formation on schwann cell  EMG/NCV

rehab aims | CHARCOT MARIE TOOTH DISEASE

Correct deformity  Improve strength  Orthotic devices

IDIOPATHICBRACHIAL NEURITIS

PARSONAGE-TURNER SYNDROME

PARSONAGE-TURNER SYNDROME commonly affects

Radial nerve  Long thoracic nerve  Suprascapular nerve Spinal Accessory Nerve Males>Females 1/3 has both shoulders affected

Sharp pain on shoulder followed by aching sensation  Weakness  Atrophy  Prognosis: Good

PARSONAGE-TURNER SYNDROME

A disease that causes degeneration and loss of the motor neuron in the spinal cord, brainstem motor nuclei and the motor cortex  Men> women  Familial in 5%- Autosomal dominant

ALS

Appears middle to late life  10% may have symptoms by age 40 yrs  No geographical or racial predilection  Invariably leads to death within a few yrs of diagnosis  Slower progression noted in patients who suffered at a younger age  Pathogenesis and etiology is unknown  Diagnosis is based on History and Proper PE  Diagnostics: EMG-NCV

ALS

Weakness, asymmetric with no sensory loss  Tongue fasciculations  Extraocular muscles are rarely involved

early onset ALS

Dysphagia  Immobility  Dyspnea  Atrophy  Occasional cramps  Dementia may occur  Emotional lability-bulbar involvement

ALs late

ALS rehab

Keep the patient at the highest level of function  Range of motion exercises  Communication devices  Assistive devices to improve ADL  Psychological support  Medications  Death may bedue to respiratory complications

A disabling disease of the anterior horn cell in the spinal cord  Caused by a picornavirus  Has 3 strains which are distinguished by antigenic strains

POLIOMYELITIS

picornavirus virus replicates at oropharynx

alimentary phase

Infective phase, seeding occurs from the lymphatic tissue picorna

lymphatic phase

virus gains access into the blood stream and migrates to the central nervous system: cervical and lumbar segments greatly affected picornavirus

viremic phase

Polioencephalitis  Decreased Tendon reflexes  Paralysis (distal and asymmetric)  Atrophy  Bulbar signs (CN IX, X most affected)  Constipation, gastric atony  Clumsiness, frequent fall, poor walking skills  Symmetrical  Affects pelvic muscles first  Pseudohypertrophy of calves  Gower’s sign  Other associated abnormalities o Scoliosis  Minor illness o Pain  Sore throat  Vomiting  Abdominal pain  Fever  Minor headache  Easy fatigability o Cardiac abnormalities-cardiac failure o Restrictive pulmonary disease o Decreased IQ ANCILLARY PROCEDURES  Muscle biopsy CPK (elevated)  Recovery may usually last up to 4 to 8 yrs EMG/NCV  Due to anterior horn cell recovery

poliomyelitis

poliomyelitis recovery due to

collateral sprouting

 Is the subsequent addition of paresis or paralysis roughly 30 yrs after the initial attack of Poliomyelitis  May occur in 25% to 60% of Polio victims  2 Broad categories:  Late Stages  Primary musculoskeletal symptoms  Dysphagia  Immobility  Dyspnea  Atrophy  Occasional cramps  Dementia may occur  Emotional lability-bulbar involvement  Post-poliomyelitis progressive muscular atrophy (PPMA)

POST POLIO SYNDROME

New onset of fatigue (80 to 90%)  Multiple joint pains  Decreased mobility due to altered body biomechanics or scoliosis  Physical decompensation following a recent weight gain or brief period of immobility owing to some form of physical trauma

PRIMARY MUSCULOSKELETAL SYMPTOMS

GOALS IN REHABILITATION OF POST POLIO

Focused on maintaining strength of the weakened muscles (those with muscle strength of 3)  Regaining function  Use of assistive device  Use of braces

Group of muscle diseases whose common primary symptom is proximal limb muscle weakness Majority has no cure Treatment is focused on:   Prevention Maximizing function

MYOPATHIES

causes MYOPATHIES

Congenital-Collagen-vascular  Metabolic-Toxic  Endocrine-secondary to other etiologies  Infectious

X linked recessive myopathy  Incidence: 1/3,500 live male births  Prevalence: 3/ 100,000 live males  1/3 of cases are due to spontaneous mutation  Severe or absent Dystrophin  Abnormality in short arm of Chrom X (Xp21 locus)  Evident at age 3-5 y/o  Polioencephalitis  Decreased Tendon reflexes  Paralysis (distal and asymmetric)  Atrophy  Bulbar signs (CN IX, X most affected)  Constipation, gastric atony  Clumsiness, frequent fall, poor walking skills  Symmetrical  Affects pelvic muscles first  Pseudohypertrophy of calves  Gower’s sign  Other associated abnormalities o Scoliosis  Minor illness o Pain  Sore throat  Vomiting  Abdominal pain  Fever  Minor headache  Easy fatigability o Cardiac abnormalities-cardiac failure o Restrictive pulmonary disease o Decreased IQ

Duchenne

ancillaru duchenne

Muscle biopsy CPK (elevated) EMG/NCV

duchenne loses ability to walk age

duchenne die at

duchenne cause of death

respiratory insufficiency

duchenne rehab aims

Maintain strength  Prevent deformities  Maintain Mobility  Maintain hand function and ADL  Fatigue should not happen!

Milder variant of DMD  X linked recessive disorder  Incidence: 1/50,000 live male births  Weakness starts at 10-15 yrs of age  Has lower amounts of Dystrophin  Prognosis: better than DMD

MUSCULAR DYSTROPHY

Weakness  Pseudohypertrophy  Cardiac abnormalities-cardiomyopathy  Gower’s sign

MUSCULAR DYSTROPHY

life expectancy muscular dystrophy

milder, may live up to 6th decade

Weakness of hips and then shoulders REHABILITATION AIMS LIMB GIRDLE DYSTROPHY  Autosomal Dominant or recessive  May also be seen as:  Sarcoglycan gene mutation has been identified in four forms  Facial muscles are spared

limb girdle

limb girdle ancillary

cpk muscle biopsy moth eaten whorled fibers emg/ncv

death limb girdle

cardiopulmo, pneumonia

an inflammatory disease of the central nervous system characterized by areas of demyelination  3rd most common cause of disabling illness between 15 and 50  1.1 million affected worldwide  More common in females  Average age of onset: 32.4 for female and 34.3 for males  Linked with Human Lymphocyte Antigen but may vary in population  Often linked with chromosome 6 however mendelian inheritance is not well established  May be confused with other diseases  Occurs as “plaques” on the white matter

Frequently seen in white matter  Prognosis is Poor if: o Male o Progressive course at onset o Age of onset >40 yrs o Cerebellar involvement at onset o Multiple system involvement at onset  Cause of Death: complication of the disease such as: o Infection o Pulmonary Embolism o Malnutrition o Dehydration o May also be due to suicide ANCILLARY PROCEDURES  CSF MRI EMG/NCV/SSEP o Near the lateral ventricle o Floor of the fourth ventricle o Corpus collosum o Periaqueductal region o Optic nerves, chiasm, tract in the corticomedullary junction o White matter tracts of the spinal cord

Inflammatory reaction with perivascular lymphocytic cuffing, local disruption of the blood brain barrier with edema, and migration of T lymphocytes and some plasma cells into the parenchyma, followed by macrophages, which appear foamy as they ingest fragmented myelin debris.  Axons spared  Chronic plaques show absent oligodendrocytes, inflammatory cells  Presumed autoimmune reaction to myelin sheath  Symptoms present at onset of illness in Definite MS: o Weakness that may be accompanied by increased muscle stretch reflexes and in the lower limbs o Paresthesia which is often painful o Optic Neuritis o Diplopia o Ataxia o Disturbed nutrition o Gait difficulty

discrete attacks produced increased neurologic impairment, which subsequently improves or resolves over ensuing weeks to months

Secondary progressive pattern

in which gradual accumulation of neurologic deficit is present from the onset of the disease without superimposed relapses

Primary progressive

in which the disease appears clinically quiescent without progression

Plateaued pattern

individuals with initial relapses and remissions have little or no neurologic deficit 1 yrs following onset. Some patients, however may later go on to develop progressive disease

Benign MS

a particularly aggressive course of primary progressive MS leading to death from fulminant disease within 5 yrs of onset

Malignant MS

MS ancillary

CSF MRI EMG/NCV/SSEP  Individualized  PREDNISONE  May decrease the length and severity of exacerbation  INTERFERON  May decrease the number of exacerbation

May decrease the length and severity of exacerbation | MS

predinisone

May decrease the number of exacerbation | MS

interferon

May slow progression inchronic MS

azathioprine

dec ataxia MS

isoniazid

Ameliorating Fatigue: | MS

amantadine | permoline (liver toxicity)

Nerve and Muscle Flashcards

(91 cards)