ergset Flashcards
-carpal tunnel
-CRPs
-GB
-DM neuropathy
-bells palsy
-oculomotor palsy
TEST
-MCC- camp jejuni
-budapest criteria dont need to know
-polyneuropathy- ignore hereditary
-lumbar sacral chart- dont need to know
-never assume neck pain radiating down to arm is MSK
complex regional pain syndrome (CRPS)
-neuropathic pain disorder
-Pathophysiology is multifactorial and involves pain dysregulation in the sympathetic and central nervous systems, with likely genetic, inflammatory, and psychological contributions. Exact mechanism is unclear.
-Occurs after fractures (MC), surgery
-Pain experienced is disproportionate to the degree of tissue injury and persists beyond the normal expected time for tissue healing.
-Pain is more regional rather than dermatomal or peripheral nerve distribution
CRPS symptoms
-SENSORY
-allodynia (usually non-painful stimuli cause pain)
-hyperalgesia (usually painful stimuli cause exaggerated pain)
-MOTOR
-weakness, reduced range of motion, tremor, and even dystonia
-AUTONOMIC
-skin color and temp changes (vasomotor dysfunction)
-swelling and sweating changes (sudomotor dysfunction)
CRPS tx
-PT/OT
-Pharmacotherapy:
-Anti-inflammatories, anticonvulsants, antidepressants, transdermal lidocaine, bisphosphonates
-Behavioral therapy
-Interventions:
-Nerve blocks
-Spinal cord stimulation
A 27-year-old female with no significant medical history presents with complaint of weakness. Symptoms have been present for the past three days. She describes initial onset of bilateral leg tingling and weakness that has progressed since onset. She awoke today and had difficulty walking so presented to the emergency department (ED). She has never had these symptoms before. She recovered from a severe diarrheal illness 2 weeks ago but denies any current gastrointestinal symptoms.
Vital signs: Temperature (T) 99.0°F, heart rate (HR) 92, blood pressure (BP) 106/78, respiratory rate (RR) 18, oxygen saturation O2sat 97% on room air.
Physical exam: The patient appears fatigued but is not in any distress. Heart is regular. Breath sounds slightly diminished but otherwise clear. Lower extremity strength is 3/5 bilaterally and patellar reflexes are absent
guillane-barre syndrome
-Autoimmune disorder causing destruction of peripheral nervous system myelin sheath/axons (somatic and autonomic) and cranial nerves causing an acute polyneuropathy
-Incidence oof 1-2 per 100,000 per year
-All age groups, but changes increase with age
-Male > Female
-Preceding infection / trigger~5 days to 4 weeksbefore the onset of neurologic symptoms
-Idiopathic 40%
-Infections – EBV, CMV, mycoplasma, campylobacter jejuni
-Immunizations – 17% of cases in one study had recent immunization
-Surgery
-Immune response to preceding infection –> molecular mimicry of peripheral nerves –> cross reaction in immune response –> demyelination
guillain barre syndrome
-2-4 weeks after a preceding illness
-!!Progressive ascending symmetric flaccid weakness (+/- diaphragm) and loss of DTRs (94%)
-Cranial nerve involvement (fascial weakness, dysphagia, dysarthria, ophthalmoplegia) (46%)
-Sensory disturbance(paresthesia/pain) (54%) is often the first symptom. Mild compared to weakness.
-Autonomic dysfunction(tachycardia, bradycardia, dysrhythmias, wide variations in blood pressure, postural hypotension, urinary retention, constipation, facial flushing, anhydrosis, hypersalivation) may be present.
-!!Cytoalbuminologic dissociationof cerebrospinal fluid (high protein andnormal white cell count)
-Severe respiratory weakness requiring mechanical ventilation occurs in about 30%
-Pain is often present in back and extremities (66%)
-Should not have brain localizing findings, or fever at onset
-Symptoms peak in ~2 weeks, nadir in 4 weeks, and recovery varies from weeks to a year
guillain barre syndrome dx
-Clinical evaluation
-Lumbar puncture: !Albumino-cytologic dissociation! (high protein (after 1 week) but normal CSF WBC count), non-emergent
-EMG/NCS: acute polyneuropathy with either demyelinating or axonal features
-Neuroimaging indicated to rule out spinal cord compression / cauda equina (mimic)
-Negative inspiratory force (NIF) testing used to predict impending respiratory failure
-Normal NIF is >60cm of water
-Abnormal NIF <30cm (or dropping from baseline); consider PPV or intubation
-Features that make dx doubtful:
-Sensory level (decrease or loss of sensation below a spinal cord root level as determined by neurologic examination)
-Marked, persistent asymmetry of weakness
-Severe and persistent bowel and bladder dysfunction
-More than 50 white cells in the CSF
guillain barre syndrome ddx
-Other acute polyneuropathies: severe vitamin B1 deficiency, acute arsenic poisoning, n-hexane (glue sniffing neuropathy), vasculitis, Lyme disease, tick paralysis (mostly in children), porphyria, sarcoidosis, leptomeningeal disease, paraneoplastic disease, and critical illness.
-Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
-Continues to progress or has relapses for greater than eight weeks.
-Diseases of the spinal cord, neuromuscular junction, and muscle.
-Distinguish from cauda equina syndrome, which is often associated with bowel/bladder disturbance, and confirmed with MRI L/S spine
guillain barre syndrome tx
-Primarily supportive
-Monitor respiratory status, prevent immobility consequences, pain management
-IVIG or Plasmapharesis
-Indicated if non-ambulatory within 4 weeks of onset, or, in ambulatory patients not improving within 4 weeks of symptom onset
neuropathies
peripheral neuropathy
-Nerves: made of many axons. Some are surrounded by a layer of myelin sheath (insulation), all bundled together with connective tissue into a giant cable.
-!!Peripheral neuropathy is frequently used synonymously with polyneuropathy, but can also refer to any disorder of the peripheral nervous system including radiculopathies and mononeuropathies.
-!Mononeuropathy refers to focal involvement of a single nerve, usually due to a local cause such as trauma, compression, or entrapment.
-Example: Carpal tunnel syndrome: a common mononeuropathy
polyneuropathy
-Wide variety of causes. Divided into axonal and demyelinating types.
-Most common : Diabetic polyneuropathy (predominantly axonal)
-Other common: alcohol abuse, and HIV infection
-Other systemic causes, predominantly axonal neuropathy:
-Critical Illness Polyneuropathy: a/w prolonged intubation and poor nutritional status
-Vitamin deficiencies
-Amyloidosis
-Hypothyroidism
-Lyme disease
-Toxic (predominantly axonal): Alcohol, Chemotherapy, heavy metals
-Hereditary- Charcot-Marie-Tooth types 1A, 1B, and X-linked, are all predominantly demyelinating.
-Idiopathic: No specific cause identified in 25%.
polyneuropathy sx
-Symmetric distal sensory loss, burning, or weakness.
-MC: Chronic axonal polyneuropathies (eg, DM or uremia)
-Injury tends to be related to axon length; thus, longer axons are affected first, resulting in symptoms that begin in the lower extremities.
-Sensory symptoms usually precede motor symptoms.
-Slowly progressive sensory loss and dysesthesias such as numbness, a burning sensation and pain in the feet, and mild gait abnormalities.
-As the syndrome progresses, mild weakness of the lower legs and hand symptoms may begin, resulting in the classic “stocking and glove” distribution of sensory loss.
-The numbness may continue to extend proximally in severe cases, affecting the intercostal nerves (the next longest nerve fibers after the arms), and causing sensory loss over the sternum.
-The top of the head may be affected with further progression.
-Early on can be identified w/ detailed sensory examination of the lower extremities
polyneuropathy: axonal neuropathy exam
-Wasting of the intrinsic muscles of the feet or lower leg (late: hands)
-Distal loss of sensation to pin prick, light touch, vibration, cold, and proprioception may also occur.
-Reflexes become hypoactive or absent distally, usually at the ankles initially.
bells palsy
-Acute peripheral facial nerve (CN VII!) palsy
-We only call it Bells if its idiopathic
-Risk increases during pregnancy:3rd trimester - first postpartum week.
-Etiology: HSV activation! (MC), then zoster
-!Sudden onset (usually over hours) of inability to close the eye, disappearance of the nasolabial fold, and mouth drawn to the unaffected side.
-May also have!decreased tearing, hyperacusis, and/or loss of taste sensation on the anterior two-thirds of the tongue!
-Onset is acute, over a day or two; the course is progressive, reaching maximal clinical weakness within three weeks
-Recovery or some degree of function is present within six months
74 yo man with DM with pain over RIGHT eyebrow x 3 days and diplopia on looking to LEFT.
Exam shows partial deficit in adduction of RIGHT eye, and inability to supraduct or infraduct (look up or down) left eye.
Pupils are symmetric and reactive.
oculomotor nerve palsy
-Oculomotor nerve palsies often present with ptosis and a “down and out eye”
-Is it an “ischemic” or “medical” 3rd nerve palsy (3NP)?
-Dilated and nonreactive: indicates a space-occupying lesion/posterior communicating artery aneurysm compressing CNIII (due to compression of external parasympathetic fibers)
-Spared pupil: indicates ischemic/inflammatory etiology as pupillary fibers run externally on nerve and have more collateral blood supply, making them less susceptible to ischemia than central nerve fibers
-Consider microvascular vasculopathy from DM (this will usually be painful)
mononeuropathies
-Damage or dysfunction of a singular peripheral nerve
-Most common: Carpal tunnel syndrome, cubital tunnel syndrome, peroneal nerve
-Causes: nerve compression against a tight or constrictive surface, entrapment of nerve in a narrow space, repetitive actions causing trauma to nerve, infections, radiation, cold
-Symptoms:
-Sensory: Numbness, tingling, pain!!
-Motor: Weakness, loss of coordination, long standing can cause atrophy!!
carpal tunnel syndrome
-Most frequent compressive focal mono neuropathy
-Prevalence : 1-5%; F > M (3:1)
-Risk factors: obesity, female
-Associated conditions: diabetes, pregnancy, rheumatoid arthritis, hypothyroidism, connective tissue diseases!!
-!Pain or paresthesia’s (numbness and tingling) in median nerve distribution (first 3 ½ fingers)
-Symptoms typically worse at night;
-!!Typical hx: shakes hand out on awakening.
-Sx may be at wrist, entire hand, or radiate proximally to as high as the shoulder.
-Sx often provoked by activities that involve flexing or extending the wrist.
-In more severe CTS, weakness or clumsiness of hand.
-Role of repetitive hand/wrist use and workplace factors in the development of CTS is controversial
carpal tunnel syndrome exam
-Motor exam usually normal
-Late stages: weakness of thumb abduction and opposition, and atrophy of the thenar eminence.
-Sensory exam: deceased sensation in median distribution!, but spares the thenar eminence (palmar sensory cutaneous nerve arises proximal to the wrist and passes over, rather than through, the carpal tunnel)
-Provocative maneuvers: Phalen, Tinel. (see slides)
-Nerve conduction studies (NCS): slowed conduction velocities across the carpal tunnel and normal conduction elsewhere.
-EMG: r/o other causes: polyneuropathy, plexopathy, and radiculopathy.
-Ddx: Cervical radiculopathy, (C6 or C7 nerve root involvement commonly mimics CTS)
-Cervical radiculopathy : neck pain, the exacerbation of sx with neck movement, radiation of pain from the neck into the shoulder and arm, reduced reflexes mediated by the C6/C7 nerve roots (ie, biceps, brachioradialis, and triceps), weakness of proximal arm muscles involving elbow flexion, extension, and arm pronation, and sensory loss in the palm or forearm outside the region of sensory abnormalities caused by CTS.
test for nerve entrapment neuropathy
-Test sensation of the nerves:
-INDEX FINGERPAD = Median nerve
-DORSAL WEBSPACE OF THUMB/INDEX = Radial nerve
-PINKY FINGERPAD = Ulnar nerve
phalen maneuver
tinel’s test
+ if shooting, aching, worsening numbness with repeated tapping
