Neurology Flashcards
Name two unique pain conditions associated with MS
Trigeminal neuralgia
Migraine headache
What kind of pain disorder can patients with SCI have?
Syringomyelia
Central Dysesthetic Pain Syndrome
Name the 4 main headaches?
Migraine
TTH
Trigeminal Autonomic Cephalalgias - Cluster
Other primary headache disorders
Name 5 medications that can cause medication overuse headache
acetaminophen, NSAIDs, ergotamine, triptans, opioids
Name two secondary headaches
reversible cerebral vasoconstrictive syndrome vertebral artery dissection SAH Venous thrombosis Spontaneous intracranial hypotension Low CSF pressure headache Idiopathic intracranial hypertension
QST is useful for what purposes?
- identification of subgroups of patients with different underlying pain mechanisms
- prediction of therapeutic outcomes
- quantification of therapeutic interventions
Name the sensory fibers associated with the components of the QST:
Cold Detection Threshold:
Warm Detection Threshold:
Vibration Detection threshold:
Cold Detection Threshold: A-delta
Warm Detection Threshold: C-fiber
Vibration Detection threshold: A-beta
The 2008 IASP definition of neuropathic pain has a grading system for neuropathic pain. What are the criterion of this grading system?
- pain distribution
- link between the distribution and the patient’s symptoms
- confirmatory neurological tests that match he sensory signs linked with the innervation territory of the lesioned nervous structure
- further confirmatory diagnostic tests to identify the lesion of disease underlying the neuropathic pain.
What are the grades of the neuropathic pain in the IASP definition?
Possible neuropathic pain
Probable neuropathic pain
Definite neuropathic pain
Increased sensitization to heat points to ______ sensitization while increased sensitization to mechanical stimuli points to _______ sensitization.
peripheral; central
In what patients is QST not appropriate?
- very young children
- mentally disabled individuals
- acutely psychotic individuals
- people with hearing impairments
- language difficulties (aphasia)
- excessively sedated
Thermoreception, nociception, and viscerorecption decussate immediately and travel up the spinal cord in the ______ and mechanorecptors and proprioceptors travel up the _____
ventrolateral STT; dorsal columns and cross over in the lower brainstem (cuneate and gracile nucleus)
QST summary:
- Cool - ____ fibers
- Warm - ____ fibers
- Cold pain - ____ fibers
- Heat pain (at threshold) - ____ fibers
- Heat pain (supramaximal) - ____ fibers
- Mechanical pain (single) - ____ fibers
- Mechanical pain (repetitive) - ____ fibers
- Mechanical non-pain (vibratory) - ____ fibers
- Mechanical (von Frey) - ____ fibers
- Current 5 Hz - ____ fibers
- Current 250 Hz - ____ fibers
- Current 2000 Hz - ____ fibers
- A-delta
- C
- A-delta+C
- C
- A-delta
- A-delta+C
- C
- A-beta
- A-beta
- C
- A-delta
- A-beta
Compare & Contrast PHN vs TN
Distribution: PHN (V1 80%) vs TN (V2/3 predom)
PHN (Herpetic lesions of face - not confined to trigeminal system, can also involve geniculate ganglion, eruption near ear) vs. TN (confined to V1-3 distribution)
Etiol: PHN (HZV preceding) vs. TN (Idiopathic)
Pathophys: TN (compression of trigeminal root of posterior fossa by superior cerebellar artery vs PHN (VZV infection into DRG + peripheral sensory nerve, w/ eventual necrosis of DRG & atrophy of dorsal horn (DH))
Assoc Symp: PHN (facial lesions) vs. TN (facial muscle spasm - tic douloureux)
Compare/contrast TN vs GN
Pain pattern: TN (V2/3 > V1) vs GN (ear, base of tongue, tonsillar fossa, beneath angle of jaw)
Pathophys: TN (compression of trigeminal root of posterior fossa by superior cerebellar artery) vs. GN (vasc impingement by the posterior cerebellar artery)
Affected nerves: TN (V) vs. GN (auricular/pharyngeal branches of IX, X)
Precipitation: TN (innocuous trivial stimuli -LT/stim to face, mouth; wash/shave/smoke/talk) vs GN (chewing, talking, swallowing, yawning, coughing)
SAME: U/L, recurrent, paroxysms, electrical shock like, shooting pain, severe intensity, duration: fraction of a sec-2 min,
EMG testing can identify injury to which anatomic sites?
- anterior horn cell
- spinal root
- plexus
- peripheral nerve
- NMJ
- muscle
EMG testing can identify injury to which types of neurons?
- sensory
- motor
- autonomic
EMG testing can determine which types of pathological injury?
- demyelination
- axonal degeneration
EMG testing can determine the time course of injury into what main categories?
- acute
- subacute
- chronic
What are the main neurophysiological entities recorded in EMG studies?
- compound muscle action potential (CMAP); motor (mV)
- sensory nerve AP (SNAP)
- amplitude
- latency (msec)
- conduction velocity (m/s)
- H reflex (soleus and flexor carpi radialis); helpful for polyneuropathies, S1 radiculopathy, UMN lesions
- F waves
EMG - what is an F wave?
- a response from a stimulus that travels first to and then from the cord vis motor pathways
- a long latency muscle AP seen after supramaximal stimulation to the nerve
- useful for studying the proximal portion of motor nerves
- Helpful in the evaluation of radiculopathy, GBS, motor neuron disease, peripheral neuropathies, entrapment neuropathies, demyelinating neuropathies
EMG - what MUAPs?
motor unit action potentials:
- the summation of the muscle fiber APs of a given motor unit
- onset frequency is the firing rate of a single MUAP maintained at the lowest frequency (<10Hz)
- recruitment freq is when the 2nd MUAP is recuited
What is seen on EMG in demyelinating disease?
- no spontaneous activity
- reduced recruitment with conduction block
- normal MUAP
- prolonged latency
- temporal dispersion
- slow NCV
What is seen on EMG in axonal injury?
- increased insertional activity and spontaneous activity
- reduced recruitment
- large amplitude, long duration polyphasics
- satellite potentials
- normal NCV latency
- slow NCV
- small CMAP/SNAP amplitude
What are the findings/changes on EMG in axonal injury (using the following neurophys entities)?
- insertional activity
- Spont activity
- MUAP amplitude
- Duration
- Phase
- Stability
- Recruitment
- amplitude
- Insertional activity - increased
- Spont activity - present
- MUAP amplitude - increased
- Duration - increased
- Phase - increased
- Stability - Normal
- Recruitment - decreased
- Amplitude - decreased
What are the findings/changes on EMG in NMJ defect (using the following neurophys entities)?
- insertional activity
- Spont activity
- MUAP amplitude
- Duration
- Phase
- Stability
- Recruitment
- Insertional activity - increased
- Spont activity - present
- MUAP amplitude - decreased
- Duration - decreased
- Phase - increased
- Stability - variable
- Recruitment - normal
What are the findings/changes on EMG in myopathic disease (using the following neurophys entities)?
- insertional activity
- Spont activity
- MUAP amplitude
- Duration
- Phase
- Stability
- Recruitment
- Insertional activity - increased
- Spont activity - present
- MUAP amplitude - decreased
- Duration - decreased
- Phase - increased
- Stability - normal
- Recruitment - increased
What changes do you see on EMG as time goes on following axonal injury (in the following categories)? 0-1 week 1-2 weeks 2-3 weeks 1-3 months 3-6 months
0-1 week - decreased recruitment 1-2 weeks - decreased recruitment - increased insertional activity 2-3 weeks - decreased recruitment - increased fibrillation potentials 1-3 months - decreased fibrillation potentials - decreased amplitude - increased duration - increased phase 3-6 months - increased recruitment - increased amplitude - increased duration - increased phase
What changes do you see on NCV as time goes on following axonal injury (in the following categories)? 0-1 week 1-2 weeks 2-3 weeks 1-3 months 3-6 months
0-1 week - decreased amplitude, proximal 1-2 weeks - decreased amplitude, proximal and distal 2-3 weeks - decreased amplitude, proximal and distal 1-3 months - increased amplitude 3-6 months - increased amplitude
What do you see on EMG in CTS?
- distal sensory conduction slowing, reduced latency
- if severe, secondary axonal damage/loss in thenar muscles
- if severe, prolonged distal latency (normal proximal) in motor studies with reduced CMAP
What is the most common neuropathy from HIV ?
DSPN - Distal symmetric polyneuropathy
HIV – what are the risk factors for developing neuropathy?
• Age • Rx w/ anti-retroviral therapy • Stavudine exposure • Lower CD4 count • Co-morbidities: o DM II • Statin Use • Substance use
Define neuropathic pain.
Pain caused by a lesion or disease of the somatosensory nervous system