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LMCC > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the pharmacological management of delirium?

A
  • Low dose, high potency antipsychotics: haloperidol has the most evidence and can be given IV or IM; alternatives include risperidone (less sedating), olanzapine (more sedating, can be anticholinergic itself), quetiapine (if EPS sensitive), aripiprazole (does not prolong QTc)
  • Benzodiazepines only used in alcohol/substance withdrawal delirium; otherwise, can worsen delirium (antipsychotics are not useful in EtOH or benzodiazepine withdrawal delirium)
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2
Q

What could be used as a reversal agent for benzodiazepines?

A

Flumazenil

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3
Q

Which way do the eyes nystagmus with cold/hot water for vestibulo-ocular reflex

A
  • Cold = FAST phase of nystagmus to the side Opposite from the cold water filled ear
  • Warm = FAST phase of nystagmus to the Same side as the warm water filled ear
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4
Q

For the oculocephalic reflex; turning head should elicit conjugate movement of gaze away from direction of turn. If not then what do you suspect?

A

brainstem function not intact

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5
Q

What are the cadiac investigations if you suspect ACS?

A

ECG, CK, troponin

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6
Q

List the GSC eye responses

A

Spontaneously (+4) To verbal command (+3) To pain (+2) No eye opening (+1)

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7
Q

What is the 4AT exam for delirium?

A

4 components: ● (1) do they wake up? If they don’t wake up within 10s, that’s an immediate fail. ● (2) Run them through 4 questions: Age, DOB, where are you, what year is it. 1 mistake = 1 point, 2 mistakes = 2 points. ● (3) Tell me the months of the year in backwards order. <7 months, 1 point, untestable = 2 points. ● (4) has there been any mental change in the last 4 hours, if yes = 4 points. ● Score >4 suggests delirium. 1-3 = -2 possible impairment, needs further assessment. 0 = unlikely but still possible

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8
Q

Initial management of coma?

A

o Initial stabilization includes: maintaining oxygenation > 96%, protecting airway (may need intubation), establishing IV access, giving saline if hypotensive, giving dextrose if hypoglycemic o Consider empiric treatment with: ▪ management for poisoning ▪ thiamine before results of laboratory tests are available if deficiency suspected ▪ IV antimicrobial therapy (after lumbar puncture if indicated) if sepsis suspected

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9
Q

What are some risk factors for delirium?

A

Dementia/brain disease, polypharmacy, elderly, organ failure, hospitalization

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10
Q

Ddx for delirium

A

Drugs (ABCD):

  • Alcohol intoxication, withdrawal, Wernicke Korsakoff
  • Anticholinergic – atropine, benztropine, scopolamine
  • Antidepressant – SSRI, TCA
  • Benzodiazepines and barbiturates
  • Cardiac – amiodarone, B blockers, digoxin
  • Dopamine agents – amantadine, levodopa

Infectious: Pneumonia, UTI, meningitis, sepsis

Metabolic - Organ Failure - hypoxia/hypercarbia, hypothermia, HTN, hypothyroidism - Electrolyte Imbalance – ketoacidosis, glucose (hypo, hyper), hyponatremia, hypernatremia, hypomagnesemia, hypercalcemia . Vitamin B12 deficiency

Structural: Hemorrhage – subarachnoid, epidural, subdural, intracerebral Stroke Tumor Abscess

Retention – Fecal and urinary

Seizure

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11
Q

What are the criterias of Confusion Assessment Method (CAM)?

A

CONFUSION ASSESSMENT METHOD (CAM) positive test argues strongly for delirium (LR 10.3) and negative test argues against delirium (LR 0.2). Positive test requires both major criteria 1+2 and either of the minor criteria 3 or 4 *AIDS* ACUTE ONSET AND FLUCTUATING CONFUSION abnormal behaviors come and go, increase/decrease severity INATTENTION difficulty focusing/difficulty following conversation (serial subtraction with distraction) DISORGANIZED THINKING rambling, irrelevant, illogical conversation SENSORIUM CHANGE (ALTERED LOC) agitated, hyperalert, lethargic, stuporous, or comatose

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12
Q

About half the cases of NMDA receptor encephalitis are due to?

A

About half of cases are associated with tumors, most commonly teratomas of the ovaries.

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13
Q

List the GSC motor responses

A

Obeys commands (+6) Localizes pain (+5) Withdrawal from pain (+4) Flexion to pain (+3) Extension to pain (+2) No motor response (+1)

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14
Q

Chronic management considerations for coma

A

▪ Enteral nutrition (EN) support is preferable to parenteral nutrition support when feasible. ▪ Tracheotomy should be considered after initial stabilization on ventilator when it becomes apparent that the patient will require prolonged mechanical ventilation. ▪ Strategies to prevent pressure ulcers include repositioning, nutritional support, and special mattresses.

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15
Q

Three subtypes of delirium?

A

Hyperactive Delirium - characterized by agitation and/or hallucinatory symptoms Mixed Delirium: variable course with alternating hyperactive and hypoactive features. A majority of patients with delirium fall under this category Hypoactive Delirium: characterized by excessive drowsiness and decreased level of consciousness. May mimic depression

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16
Q

What is Lewy-Body Dementia?

A

Dementing process characterized by fluctuations in LOC, hallucinations, and parkinsonism (stiff, slow, usually no tremors). Patient with this are very sensitive to neuroleptics (can become very parkinsonian).

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17
Q

What breathing pattern might you see you a diencephalon injury?

A

Cheyne-Stokes

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18
Q

List the GSC verbal responses

A

Oriented (+5) Confused (+4) Inappropriate words (+3) Incomprehensible sounds (+2) No verbal response (+1)

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19
Q

Sx of normal pressure hydrocephalus

A

Wet, wacky, and wobbly - Triad of dementia, gait disturbance and urinary incontinence

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20
Q

How to perform Hoffman’s Reflex

A

Sitting or standing, support arm, grab inferiorly the middle finger proximal to the DIP and flick the patient’s distal phalanx downward (+) UMN Lesion = pincher movement of index and thumb

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21
Q

What could be used as a reversal agent for opioids?

A

Naloxone

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22
Q

What are the symptoms of NMDA receptor encephalitis?

A

Often present with subacute onset psychiatric symptoms (delusions, hallucinations, catatonia). People are also often agitated or confused. Over time seizures, decreased breathing, and blood pressure and heart rate variability typically occur.

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23
Q

What is unique about the gait in normal pressure hydrocephalus

A

Gait is unique – cant lift legs off ground, but if lying down can mimic walking

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24
Q

What are the investigations (basic) you would do for delirium?

A

LABS CBCD, lytes, urea, Cr, glucose, Ca, urinalysis IMAGING CXR, head CT MICROBIOLOGY urine C&S, blood C&S (if any fever)

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25
Q

Mnenomic for GCS

A

My Extra Value Meal costs $4.56

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26
Q

What is NMDA receptor encephalitis?

A

It is an autoimmune disease, where the body creates antibodies against the NMDA receptors in the brain. These antibodies disrupt normal brain signaling and cause brain swelling, or encephalitis.

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27
Q

What is Non-Convulsive Status Epilepticus?

A

Recurrent or continuous subclinical seizures resulting in a fluctuating or diminished level of consciousness. Electrographic seizures seen on EEG with little or no obvious motor manifestations of seizure. Think of this when a person has ongoing delirium with no identifiable cause. EEG when suspicion.

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28
Q

Investigations for coma?

A

o Initially, pulse oximetry, fingerstick plasma glucose measurements, and cardiac monitoring are done. o Blood tests should include a comprehensive metabolic panel (including at least serum electrolytes, blood urea nitrogen [BUN], creatinine, and calcium levels), complete blood count (CBC) with differential and platelets, liver tests, and ammonia level. o Arterial blood gases (ABGs) are measured, and if carbon monoxide toxicity is suspected, carboxyhemoglobin level is measured. o Blood and urine should be obtained for culture and routine toxicology screening; serum ethanol level is also measured. o ECG + CXR + EEG (seizures) o If the cause is not immediately apparent, noncontrast head CT should be done o If coma is unexplained after MRI or CT and other tests, lumbar puncture (spinal tap) is done to check opening pressure and to exclude infection, subarachnoid hemorrhage, and other abnormalities

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29
Q

What would you suspect for cerebral and brainstem damage with the vestibulo-ocular reflex?

A

▪ Cerebral Damage: fast phase absent, deviation to same side if cold water ▪ Brainstem Damage: fast + slow phase absent

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30
Q

Tx of normal pressure hydrocephalus

A

Treat with CSF drain (30-40 cc’s) and place a VP shunt

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31
Q

Definition of coma

A

Coma refers to a state of unresponsiveness without arousal caused by interruption of neuronal networks that regulate consciousness.

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32
Q

What are the investigations if you suspect liver disease?

A

AST, ALT, ALP, bilirubin, INR, PTT, NH4

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33
Q

Physical exam of coma?

A

General: neck flexion, breath odor, look for head trauma Neuro: LOC, GCS, oculocephalic reflex, CN (pupils, corneal reflex, gag reflex), reflexes (Babinski’s and Hoffman’s), tone

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34
Q

What are the neurological mimics of delirium?

A

Non-Convulsive Status Epilepticus Aphasia Lewy-Body Dementia Encephalitis

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35
Q

What is the environmental management of delirium?

A
  • environment: quiet, well-lit, near window for cues regarding time of day - optimize hearing and vision - room near nursing station for closer observation; constant care if patient jumping out of bed, pulling out lines - family member present for reassurance and re-orientation - frequent orientation: calendar, clock, reminders - avoid frequent changes of assigned nursing staff
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36
Q

Ddx of coma

A

GAMETIMES: o G - Hyperosmolar + Hypo/hyperglycemia o A - Anoxia + Acidosis + Alcohol + Aneurysm o M - Meds + Drugs (alcohol, anesthetics, opioid, sedatives, SSRI, cocaine) o E – Electrolytes (hypercalcemia, hyper/hyponatremia) + Environment (Hypo/hyperthermia, hypoxia) o T - Tumor + Toxin (CO) + Trauma (Subarachnoid Hemorrhage, Subdural Hematoma) o I – Infections (encephalitis, malaria, meningitis) o M - Metabolic + Adrenal + Renal + Hepatic o E – Epilepsy (focal) o S - Stroke + Psychiatric

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37
Q

Pathophysiology of hearing loss?

A
  1. Conductive Hearing Loss - Conduction of sound to the cochlea is impaired. 2. Sensorineural Hearing Loss - Defect in the conversion of sound into neural signals or in the transmission of those signals to the cortex 3. Mixed Hearing Loss - Combination of CHL and SNHL
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38
Q

Most common causes of hearing loss?

A

Cerumen accumulation, Noise, Aging (Presbycusis), Infections (particularly among children and young adults)

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39
Q

Congenital causes of hearing loss?

A

Conductive: Genetic, Developmental (eg, ossicular fixation), Idiopathic (unknown) malformation, Drug-induced malformation (eg, with thalidomide) Sensory: Genetic, Idiopathic (unknown) malformation, Congenital infection (eg, rubella, cytomegalovirus infection, toxoplasmosis, syphilis), Rh incompatibility, Anoxia, Maternal ingestion of ototoxic drugs (eg, for tuberculosis or severe infection), Drug-induced malformation (eg, with thalidomide) Neural: Anoxia, Idiopathic (unknown) malformation, Genetic, Congenital infection (eg, rubella, cytomegalovirus infection, toxoplasmosis, syphilis), Neurofibromatosis (type 2), Hyperbilirubinemia

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40
Q

Acquired causes of hearing loss?

A

External ear (conductive loss): Obstruction (eg, caused by cerumen, a foreign body, otitis externa, or, rarely, tumor) Middle ear (conductive loss): otitis media, ear trauma, otosclerosis, tumors Inner (sensory loss): Genetic disorders (eg, connexin 26 mutation – most common), noise exposure, presbycusis, ototoxic drugs (eg, aspirin, aminoglycosides), infections (eg, meningitis, purulent labyrinthitis), Meniere syndrome, barotrauma CNS (neural loss): Tumors of the cerebellopontine angle (eg, acoustic neuroma, meningioma - tinnitus), Demyelinating disease (eg, multiple sclerosis)

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41
Q

What is otosclerosis and age of onset

A

Abnormal bone growth inside the ear, FHx, age of onset 20-30s

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42
Q

Waardenburg syndrome signs

A

White forelock of hair or different colored eyes

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43
Q

Pendred syndrome signs

A

Associated with thyroid gland disorders, SLC26A4 gene, enlarged vestibular aqueducts

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44
Q

High Risk Factors for hearing loss in newborns

A

Low birthweight/prematurity, perinatal anoxia (low APGARs), kernicterus:bilirubin >25mg/dL, craniofacial abnormality, family history of deafness in childhood, 1st trimester illness: TORCH infections, neonatal sepsis, ototoxic drugs, perinatal infection, including post-natal meningitis, consanguinity

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45
Q

Who should be screened for hearing loss

A

All infants

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46
Q

Important history points for hearing loss

A

Should note how long hearing loss has been perceived, how it began (eg, gradual, acute), whether it is unilateral or bilateral, and whether sound is distorted (eg, music is off—dull or lifeless) or there is difficulty with speech discrimination. Any acute event. other otologic symptoms (eg, ear pain, tinnitus, ear discharge), vestibular symptoms (eg, disorientation in the dark, vertigo), and other neurologic symptoms (eg, headache, weakness or asymmetry of the face, an abnormal sense of taste, fullness of the ear).

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47
Q

What should be included for the physical exam of hearing loss?

A

External ear + TM inspection, Neuro exam (particular attention needs to be paid to the 2nd through 7th cranial nerves). Weber + Rhine testing

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48
Q

Which cranial nerves are also affected by tumors that involve the 8th nerve

A

The 5th or 7th cranial nerve or both are often affected by tumors that involve the 8th nerve, so loss of facial sensation and weak jaw clench (5th) and hemifacial weakness and taste abnormalities (7th) point to a lesion in that area

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49
Q

How is the weber test performed?

A

512 Hz tuning fork is held on vertex of head and patient states whether it is heard centrally (Weber negative) or is lateralized to one side (Weber right, Weber left)

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50
Q

Weber Test lateralization

A

Weber Test lateralization = ipsilateral conductive hearing loss or contralateral sensorineural loss

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51
Q

Weber = lateralizes to left Rinne = AC>BC (+) bilaterally

A

Right-sided SNHL, normal left ear

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52
Q

Weber = central Rinne = AC>BC (+) bilaterally

A

Normal or bilateral SNHL

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53
Q

What is the Rinne test. What’s normal?

A

512 Hz tuning fork is struck and held firmly on mastoid process to test bone conduction (BC); the tuning fork is then placed beside the pinna to test air conduction (AC), If AC > BC = positive Rinne (normal)

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54
Q

Puretone pattern for conductive hearing loss?

A
  • BC in normal range - AC outside of normal range - Gap between AC and BC thresholds >10dB (an air-bone gap)
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55
Q

Puretone pattern for sensorineural hearing loss?

A
  • Both air and bone conduction thresholds below normal - Gap between AC and BC <10 dB (no air-bone gap)
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56
Q

Puretone pattern for mixed hearing loss?

A
  • Both air and bone conduction thresholds below normal - Gap between AC and BC threshold s>10dB (an air-bone gap)
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57
Q

What is presbycusis?

A

SNHL associated with aging (starting in 5th and 6th decades)

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58
Q

Clinical features of presbycusis?

A
  • Progressive, bilateral hearing loss initially at high frequencies, then middle frequencies - Loss of discrimination of speech, especially with background noise present – patients describe people as mumbling - Recruitment phenomenon: inability to tolerate loud sounds - Tinnitus
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59
Q

Tx of hearing loss

A
  • Stop ototoxic meds - Fluid from middle ear effusion can be drained by myringotomy and prevented from reaccumulating with the insertion of a tympanostomy tube. - Damage to the tympanic membrane or ossicles or otosclerosis may require reconstructive surgery. Brain tumors causing hearing loss may in some cases be removed or radiated and hearing preserved. - Many causes of hearing loss have no cure, and treatment involves compensating for the hearing loss with hearing aids and, for severe to profound loss, a cochlear implant
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60
Q

Prevention of hearing loss

A

Prevention of hearing loss consists mainly of limiting duration and intensity of noise exposure. People required to expose themselves to loud noise must wear ear protectors (eg, plastic plugs in the ear canals or glycerin-filled muffs over the ears).

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61
Q

Delirium vs dementia

A
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62
Q

What is a primary headache?

A

No identifiable cause

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63
Q

What is a secondary headache?

A

Underlying etiology present

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64
Q

What should be included on hx for a patient with a headache?

A
  • Onset (episodic vs chronic)
  • Associated sx (visual changes, change in mental status, nausea/vomiting, fever, meningismus, photophobia, phonophobia)
  • Precipitating/alleviating factors (triggering factors, analgesics), medications (especially nitrates, calcium channel blockers, NSAIDs, anticoagulants), PMHx, FHx
  • Lifestyle factors (caffeine, exercise – regular exercise is the best prophylaxis, sleep)
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65
Q

Physical exam for a patient presenting with headache?

A
  • Vitals: is there fever? Is there severe HTN (sBP >180 or dBP >120)?
  • Fundoscopy
  • Focal Neuro Exam
  • Is there papilledema? Consider carotid artery dissection
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66
Q

What are the red flags for headache?

A

SNOOPED

  • Systemic Signs/Symptoms: papilledema, neck stiffness, immunocompromised, personality change
  • Neurologic symptoms (focal neuro deficits)
  • Old age (>50)
  • Onset is sudden or worst ever or thunderclap
  • Pattern is progressive or new
  • Evoked by valsalva, exercise, certain positions (lying down), or post-trauma
  • Daily
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67
Q

When is neuroimaging (CT) required for headaches?

A

If red flags or risk of herniation (i.e. intracranial pathology)

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68
Q

When would you use MRI w/ or w/o contrast for headache?

A

If immunocompromised, if >60 with suspect temporal arteritis

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69
Q

When would you do a lumbar puncture with a patient presenting with headache?

A
  • If suspect infection (WBCs), bleeding (RBCs), or malignancy (abnormal cells)
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70
Q

Predictors of migraine Dx

A

POUND: Pulsating/throbbing, 4-72 hOurs, Unilateral, Nausea/vomit, Disabling

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71
Q

Criteria for migraine headache

A

2/3: nausea/vomiting, photophobia, or worse w/ exercise

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72
Q

How might a migraine headache present in children?

A

Cyclical vomiting, episodic stomach pain.

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73
Q

Two types of migraine headaches?

A
  1. Aura
  2. Without aura
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74
Q

Symptoms of aura headache?

A

5-60 mins (if longer than 60 mins – get CT scan) - visual disturbance (fortification spectra - zigzags; scintillating scotomata - spots), unilateral paresthesia and numbness, dysphasic speech – NOT MOTOR WEAKNESS

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75
Q

What is cortical spreading depression?

A

Cortical spreading depression (CSD) is a propagating wave of depolarization of neurons and glial cells that spreads across cerebral cortex. The spreading of this wave is hypothesized to activate the trigeminal nerve afferents, causing inflammatory changes in pain-sensitive structures that create migraine headache

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76
Q

What are some lifestyle changes for the treatment of headaches?

A

Lifestyle (caffeine – drink same amount everyday, sleep – change in hours of sleep triggers, diet, triggers, exercise), headache diary + stress management

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77
Q

What is the hierarchy for abortive treatment for headache?

A

Hierarchy: Ibuprofen, naproxen, Tylenol → triptans → naproxen sodium + triptan, narcotic analgesic are not recommended.

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78
Q

When should a patient use abortive therapy?

A

Use at headache onset and hit it hard, not daily otherwise you can make their migraine transform to daily.

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79
Q

When is prophylactic medication indicated for migraines?

A

Indicated if headache >3 days/month and acute meds not effective OR >8 days/month OR Disability despite acute meds

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80
Q

What are 1st line prophylactic treatments for headaches?

A

1st line: propanolol, metoprolol (avoid in asthma), amitryptiline (consider if depression, anxiety, insomnia)

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81
Q

What are 2nd line prophylactic treatments for headaches?

A

2nd line: topiramate (1st line if overweight), candesartan (avoid in pregnancy)

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82
Q

What are other prophylactic treatments for headaches?

A

Other: divalproex sodium (avoid in pregnancy), pizotifen (monitor for somnolence and weight gain), botox (chronic headache only)

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83
Q

Symptoms of tension headaches?

A

Squeezing sensation (tight-band), bilateral, fronto-occipital or generalized, no N/V, no photophobia, no migrainous Sx, not worse with activity

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84
Q

What is defined as chronic tension headaches?

A

>15 days/month for >6 months

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85
Q

What are the abortive and prophylactic treatments of tension headaches?

A

Rest and relaxation

Abortive Tx with OTC meds (ibuprofen, ASA, acetaminophen, limit 2-3x/ week)

Prophylactic Tx if severe (1st line – amitriptyline, 2nd – venlafaxine (Effexor))

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86
Q

What are the symptoms of cluster headaches?

A

Severe, unilateral headaches (retro-orbital) associated with autonomic Sx (tearing, nasal congestion, rhinorrhea, conjunctivitis, horner’s syndrome, agitation), once begin often recur daily for several weeks (cluster) @ same time everyday (classically awakens @ night), <3h

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87
Q

What are the abortive and prophylactic treatments of cluster headaches?

A

Abortive: triptans, oxygen 100%

Preventative: verapamil 120-900mg – get ECG, lithium carbonate, valproate, topiramate, melatonin

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88
Q

What is transitional treatment for cluster headaches and when is it used?

A

If more than two attacks per day, consider transitional therapy while verapamil is built up (e.g., prednisone 60 mg for five days, then reduced by 10 mg every two days until discontinued, or occipital nerve blockage with steroids)

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89
Q

What is the presentation of increased ICP?

A

Consistent headache worse in AM, whooshing in ears, papilledema + focal neuro deficits

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90
Q

Who does increased ICP usually affect?

A

Typically in young overweight women

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91
Q

What do you need to rule out with increased ICP sx and with what test?

A

CT venogram (rule out venous sinus thrombosis)

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92
Q

Treatment for increased ICP

A

Steroids/repeat LP until optic nerve fenestration completed. Diamox – acetazolamide (reduces CSF produced), topiramate (helps with weight loss), weight loss, urgent referral to ophtho and neuro.

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93
Q

Sx of thunderclap headache?

A

Acute onset, reaches max intensity within minutes, worse with exertion

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94
Q

Causes of thunderclap headache

A

Causes: SAH and arterial dissection

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95
Q

Sx of meningitis and/or encephalitis?

A

Fever/chills, nuchal rigidity, photophobia, N/V, confusion/altered LOC, rash, immunocompromised

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96
Q

Sx of temporal arteritis

A

50yo localized headache (temporal), jaw claud, scalp tenderness tender temporal artery, PMR association, visual symptoms.

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97
Q

Investigations for temporal arteritis?

A

Temporal artery biopsy and CRP.

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98
Q

Tx for temporal arteritis?

A

Immediate high-dose moderate corticosteroids (prednisone)! Can lead to permanent blindness.

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99
Q

What is considered medication overuse for headaches?

A
  • Ergots, triptans, combination analgesics or codeine/other opioids ≥ 10 days a month OR
  • Acetaminophen or NSAIDs ≥ 15 days a month
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100
Q

What are the indications for urgent LP?

A
  • Suspected CNS infection (with the exception of brain abscess or a parameningeal process).
  • Suspected SAH in a patient with a negative CT scan
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101
Q

What are some contraindications for LP?

A
  • Possible raised intracranial pressure (ICP) with risk for cerebral herniation
  • Thrombocytopenia or other bleeding diathesis, including ongoing anticoagulant therapy
  • Suspected spinal epidural abscess
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102
Q

Definition of stroke?

A

Sudden onset of neurological deficits of a vascular etiology with infarction of CNS tissue

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103
Q

Definition of TIA?

A
  • Sudden onset of focal neurological deficits lasting < 24hrof a vascular etiology without infarction (i.e. no imaging evidence of stroke). May present with amaurosis fugax (transient monocular painless vision loss)
  • Tissue based definition: Rapidly resolving neurologic symptoms, typically lasting <1 hour, with no evidence of infarction on MRI (DWI – Diffusion Weighted Imaging)
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104
Q

Two types of stroke?

A
  • Ischemic (85%)
  • Hemorrhagic (15%)
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105
Q

Etiology/causes of ischemic stroke?

A
  • Arterial thrombosis: thrombus formation in artery (local/in situ)
    • Large vessel: stenosis or occlusion of the internal carotid artery, vertebral, or intracranial arteries
    • Small vessel/lacunar
  • Cardioembolic: blockage of cerebral arterial blood flow due to particles originating from a cardiac source
    • Atrial fibrillation (most common), rheumatic valve disease, prosthetic heart valves, recent MI, fibrous and infectious endocarditis
  • Systemic hypoperfusion (global cerebral ischemia): Inadequate blood flow to brain, usually secondary to cardiac pump failure (e.g. cardiac arrest, arrhythmia, or MI)
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106
Q

Etiology/causes of hemorrhagic stroke?

A
  • Intracerebral (HTN, amyloid angiopathy, other)
    • Hypertensive (most common): rupture of small microaneurysms (Charcot-Bouchard aneurysms) causing intraparenchymal hemorrhage
    • Other: trauma, amyloid angiopathy (associated with lobar hemorrhage), vascular malformations, vasculitis, drug use (cocaine or amphetamines)
  • Subarachnoid
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107
Q

ACA stroke syndrome?

A

Contralateral leg paresis, sensory loss, cognitive deficits (e.g. apathy, confusion, and poor judgment). Right hemi – neglect. Left hemi – aphasia. Sensory loss + incontinence

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108
Q

Systemic hypoperfusion primarily affects which areas?

A

Primarily affects watershed areas (between the major cerebral arterial territories)

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109
Q

Mechanism by which small vessel/lacunar causes a stroke?

A

Chronic HTN and DM cause vessel wall thickening and decreased luminal diameter

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110
Q

MCA stroke syndrome?

A
  1. contralateral weakness and sensory loss of face and arm
  2. cortical sensory loss
  3. may have contralateral homonymous hemianopia or quadrantanopia
  4. if dominant (usually left) hemisphere: aphasia
  5. if non-dominant (usually right) hemisphere: neglect
  6. eye deviation towards the side of the lesion (away from the weak side)
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111
Q

PCA stroke syndrome?

A
  1. contralateral hemianopia or quadrantanopia
  2. midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis
  3. thalamic findings: sensory loss, amnesia, decreased LOC
  4. if bilateral: cortical blindness or prosopagnosia
  5. hemiballismus
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112
Q

Proximal basilar artery stroke syndrome?

A

Proximal (usually thrombosis): impaired EOM, vertical nystagmus, reactive miosis, hemi- or quadriplegia, dysarthria, locked-in syndrome, coma

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113
Q

Distal basilar artery stroke syndrome?

A

Distal (usually embolic, i.e. top of the basilar syndrome): somnolence, memory and behaviour abnormalities, oculomotor deficit

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114
Q

PICA (lateral medullary or Wallenberg syndrome) stroke syndrome?

A

Ipsilateral ataxia, ipsilateral Horner’s, ipsilateral facial sensory loss, contralateral limb impairment of pain and temperature sensation, nystagmus, vertigo, nausea/vomiting, dysphagia, dysarthria, hiccups

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115
Q

Medial medullary infarct stroke syndrome?

A

Contralateral hemiparesis (facial sparing), contralateral impaired proprioception and vibration sensation, ipsilateral tongue weakness

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116
Q

Subcortical/lacunar infarcts stroke syndrome?

A

Contralateral weakness without cortical deficits since the stroke is now subcortical. Face/arm/leg equally involved.

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117
Q

Small vessel occlusions are lacunar strokes (20%) due to ______ (vessels thicken usually from HTN, DM2).

A

Lipohyalinosis

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118
Q

General assessment/physical exam for stroke/TIA?

A
  • ABCs, full vital sign monitoring, capillary glucose, urgent CODE STROKE if <4.5h from symptom onset (for possible thrombolysis)
  • LOC (knows age, month; obeys commands), dysarthria, dysnomia (cannot name objects)
  • Gaze preference, visual fields, facial palsy
  • Arm drift, leg weakness, ataxia
  • Sensation to pinprick, extinction/neglect
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119
Q

Mimics to rule out for stroke/TIA?

A

Seizure/post-ictal, hypoglycemia, migraine, conversion disorder

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120
Q

Investigations for stroke/TIA?

A
  • Non-contrast CT head (STAT): to rule out hemorrhage and assess extent of infarct
  • ECG: to rule out atrial fibrillation (cardioembolic cause), Holter monitor
  • CTA, carotid dopplers, ECG, transthoracic echo
  • CBC, electrolytes, creatinine, partial thromboplastin time/international normalized ratio (aim for <1.7), blood glucose (>2.7 rules out hypoglycemia), lipid profile, platelets (>100 for treatment)
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121
Q

CT imaging findings of ischemic stroke?

A

Early ischemic changes: loss of cortical grey-white matter differentiation, hyperdense vessels, sulcal effacement (i.e. mass effect decreases visualization of sulci). Later ischemia changes: hypodense of parenchyma

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122
Q

Hemorrhagic stroke CT imaging findings

A

Hyperdense. Diffusion weighted MRI is WAY BETTER than CT. The white areas on MRI showing the stroke are demonstrations of acute ischemia, which causes loss of oxygen and therefore ATPase shuts down, restricted diffusion of water out of ischemic tissue (cytotoxic edema) – this shows up as bright on the scan and can last for 4wks!

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123
Q

Acute stroke management includes?

A
  1. Thrombolysis
  2. Anti-Platelet Therapy
  3. Acute Anti-Coagulant Therapy
  4. Intra-Arterial Mechanical Thrombectomy
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124
Q

rtPA (recombinant tissue plasminogen activator) should be given within ___ of acute ischemic stroke onset provided there are clinical indications and no contraindications to use

A

4.5 h

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125
Q

Contraindications to rtPA (recombinant tissue plasminogen activator)?

A
  • Hx: improving Sx, minor Sx, seizure at stroke onset, recent major surgery or trauma (within 14 d), recent GI or urinary hemorrhage (within 21 d), recent LP or arterial puncture at noncompressible site, PMHx of ICH, Sx of SAH/ pericarditis/MI, pregnancy
  • P/E: sBP >185, dBP >110, aggressive treatment to decrease BP, uncontrolled serum glucose <2.7, thrombocytopenia
  • Labs: hemorrhage or mass on CT, high INR or aPT >1.7
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126
Q

Who should receive ASA for stroke and what is the loading dose?

A
  • Loading dose of antiplatelets at presentation of TIA or stroke if rtPA not received
  • Loading dose of ASA: recommended dose 160 mg chewed
  • If patient intolerant to ASA, use another antiplatelet agent (e.g. clopidogrel 300 mg)
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127
Q

For patients with TIA or stroke and atrial fibrillation, if rtPA not received:

A
  • recommend IV heparin (or ensuring international normalized ratio between 2-3 if already anticoagulated on warfarin)
  • may delay initiation of oral anticoagulation depending on size of infarct and presence of petechial/frank hemorrhage
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128
Q

Eligibility for early thrombectomy

A

CT angio needed to document LVO and: <6 hrs – patients must have small to moderate core on non-contrast. >6 hrs with CTP selection. Up to 24hrs!!

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129
Q

Other acute management issues for stroke?

A
  • Avoid hyperglycemia which can increase the infarct size
  • Lower temperature if febrile (febrile stroke: think septic emboli from endocarditis)
  • Prevent complications
    • NPO if dysphagia (to be reassessed by SLP)
    • DVT prophylaxis if bed-bound
    • initiate rehabilitation early
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130
Q

Blood pressure control for stroke?

A
  • Do NOT lower the blood pressure unless the HTN Is severe
  • Antihypertensive therapy is withheld for 48-72h (permissive hypertension) after thromboembolic stroke unless sBP >220 mmHg or dBP >120 mmHg, or in the setting of acute MI, renal failure, aortic dissection (IV labetalol first-line if needed)
  • Acutely elevated BP is necessary to maintain brain perfusion to the ischemic penumbra
  • Most patients with an acute cerebral infarct are initially hypertensive but their BP will improve within 1-2 d
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131
Q

Top 6 symptoms likely to be TIA?

A

*1. Hemibody Weakness – TIA until proven otherwise

*2. Speech Disturbance: for a defined period of time (definite dysarthria, muteness or marked word finding difficulty, paraphasic speech)

  1. Monocular or Hemifield Visual Loss: not blurring of entire visual field
  2. Double Vision, Crossed Numbness or Weakness, Slurred Speech, Ataxia of Gait. Localizes to the brainstem.
  3. Hemibody Numbness
  4. Vertigo: only if present with brainstem sx
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132
Q

Symptom unlikely to be TIA?

A

Positional and recurrent numbness of one limb or tingling of all 4 extremities. Scintillating or flashing visual disturbances. Symptoms of durations < 30 seconds. Seizure of convulsions at onset. Isolated syncope. Postural dizziness alone.

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133
Q

Features supportive of TIA/Stroke?

A

Well-defined onset time, definite focal neurological symptoms, presence of neurological signs on examination, being able to lateralize signs to the left or right side of the brain, being able to determine a clinical stroke subclassification

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134
Q

What is the ABCD2 Risk Score?

A

Age (>60), BP (>140/90), *Clinical Features (unilateral weakness w/ or w/o speech disturbance get 2 points or speech deficit w/o weakness), Duration (>10min < 59 min get 1 point, >60 min get 2 points), Diabetes

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135
Q

Highest risk TIA is defined as?

A

TIA symptoms in the last 48 hours with high risk sx (speech disturbance or weakness of the face, arm or leg) or lower risk symptoms (hemianopsia, monocular visual loss, brainstem syndrome)

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136
Q

High risk TIA is defined as?

A

TIA symptoms in the last 48 hours to 2 weeks with high risk sx (speech disturbance or weakness of the face, arm or leg)

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137
Q

Moderate risk TIA is defined as?

A

TIA symptoms in the last 48 hours to 2 weeks with lower risk symptoms (hemianopsia, monocular visual loss, brainstem syndrome)

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138
Q

Lower risk TIA is defined as?

A

TIA symptoms more than 2 weeks ago regardless of symptoms

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139
Q

Immediate actions for highest risk TIA?

A

Emergent assessment (brain and vascular imaging – CTA neck vessels or carotid doppler) should be done within hours. Immediate EKG and antiplatelet therapy.

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140
Q

Immediate actions for high risk TIA?

A

24 hours to get a clinical assessment done and then vascular imaging and brain imaging. EKG and immediate antiplatelet therapy.

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141
Q

Immediate actions of moderate risk TIA?

A

Investigation by a stroke expert within two weeks of first contact. Brain imaging and vascular imaging within 2 weeks. EKG and immediate antiplatelet therapy.

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142
Q

Immediate actions of lower risk TIA?

A

Referral to clinic with neurological expertise to be seen within 1 month

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143
Q

Post-TIA treatment?

A

ASA + clopidogrel given for 30 days post high risk TIA reduces recurrent stroke risk. Usually, beyond 30 days we stop clopidogrel and keep them on ASA long term

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144
Q

Secondary prevention of ischemic stroke anti-platelet therapy?

A
  • Initial choice: ASA
  • If cerebrovascular symptoms while on ASA or if unable to tolerate ASA: Aggrenox, clopidogrel
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145
Q

Secondary prevention of ischemic stroke carotid stenosis?

A
  • Carotid endarterectomy clearly benefits those with symptomatic severe stenosis (70-99%), and is less beneficial for those with symptomatic moderate stenosis (50-69%)
  • See significant reduction in stroke prevention if done w/n 6 months of symptoms.
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146
Q

Secondary and primary prevention of ischemic stroke atrial fibrillation?

A
  • Primary and secondary prevention with anticoagulation
    • All patients with atrial fibrillation without contraindication be anticoagulated
  • Anticoagulation therapy
    • warfarin (titrate to international normalized ratio 2-3)
    • dabigatran (110 or 150 mg PO bid), apixaban (2.5 or 5 mg PO bid) or rivaroxaban (15 or 20 mg PO daily) may be alternatives to warfarin, but should be used cautiously
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147
Q

Secondary and primary prevention of ischemic stroke HTN?

A
  • Primary prevention
    • Targets: BP <140/90 (sBP <120 for high risk without diabetes or <130/80 for diabetics or renal disease)
    • ACEI: ramipril 10mg PO OD is effective in patients at high risk for cardiovascular disease
  • Secondary prevention
    • ACEI and thiazide diuretics are recommended in patients with previous stroke/TIA
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148
Q

Secondary and primary prevention of ischemic stroke hypercholesterolemia?

A
  • Primary prevention: statins in patients with CAD or at high risk for cardiovascular events, even with normal cholesterol
  • Secondary prevention: high dose atorvastatin but lower doses may be adequate if patient cannot tolerate high dose
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149
Q

Secondary and primary prevention of ischemic stroke smoking?

A
  • Primary prevention: smoking increases risk of stroke in a dose-dependent manner
  • Secondary prevention: after smoking cessation, the risk of stroke decreases to baseline within 2-5yr
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150
Q

Etiology of gait disturbances?

A
  1. Cerebellar ataxia
  • Tumors
  • Vascular
  • Hereditary
  • Multiple sclerosis
  • Drugs
  • Alcohol
  1. Sensory ataxia
  • Vestibular
  • Proprioceptive
  • Visual
  1. Other disorders of locomotion
  • Other central nervous system (e.g., cerebral)
  • Parkinson’s disease
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151
Q

Physical exam for gait disturbance?

A
  • Full neurological exam
  • Coordination exam
    • finger-to-nose, heel-to-shin, knee taps, rapid alternating movements
  • Stance and gait
    • Posture, stride length, width between feet, height of step, stability of pelvis, symmetry, arm swing, difficulty turning, tremor, elaborate/inconsistent movements, standing from sitting
    • Romberg test
    • pull test or push and release test for postural instability
    • gait: antalgic, hemiplegic, ataxic, apraxic, Parkinsonian gait, steppage gait, broad-based
    • tandem gait (heel-to-toe test)
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152
Q

Red flags of gait disturbance?

A

Sudden onset, cerebellar ataxia, paresis (hemi-, para- or quadri-), bowel/bladder incontinence

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153
Q

What is an antalgic gait?

A

Painful limb, decreased stance phase; quick/short steps

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154
Q

What is a high steppage/foot drop gait?

A

Distal weakness esp. dorsiflexors, difficulty clearing toes in swing phase→ audible double slap

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155
Q

What is a spastic hemiplegic gait?

A

As a result of spasticity – UMN lesions - knee extension + plantar flexion, difficulty clearing toes in swing phase→ circumduction gait due to the weakness of distal muscles and extensor hypertonia in LL

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156
Q

What is a Trendenburg gait?

A

Proximal muscle weakness of hip abductors, pelvis excessively drops on unaffected limb during swing, to clear toes→ excessively laterally bend trunk on affected side

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157
Q

What is a waddling gait?

A

When the trendelenburg gait is bilateral in conditions such as Muscular dystrophies or Myopathies then they demonstrate bilateral excessive lateral trunk bending

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158
Q

What is an ataxic gait?

A

Unsteady on feet→ is wide based (patients overshoot or undershoot with each step.)

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159
Q

What is an parkinsonian gait?

A

Slow start, trunk bent forward, legs and arms stiff with short shuffling steps (aka festinating)

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160
Q

What is a scissoring gait?

A

Increased muscle tone in hip adductors. Leg crosses the midline in swing phase and effects balance and stability. Base is very narrow. To compensate the trunk movements.

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161
Q

Clinical features of myopathy?

A

Muscle disease, weakness is generally proximal and symmetrical (patients have problems reaching for high objects, getting up from chairs and going up stairs). Tredelenberg gait

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162
Q

Etiology of myopathies related to gait disturbance?

A

Muscular dystrophy, autoimmune disorders, myasthenia gravis (neuromuscular junction)

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163
Q

Clinical features of neuropathy?

A

Nerve disease, distal weakness and sensory change in polyneuropathy – ‘glove and stocking’. Gait pattern is related to both weakness and sensory change. High steppage gait

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164
Q

Etiology of neuropathies related to gait disturbance?

A

Diabetic neuropathy, hereditary neuropathies (Charcot-Marie-Tooth Disease), Guillian Barre syndrome, peroneal n. injury, L5 radiculopathies

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165
Q

Etiology of Parkinsonism gait?

A

PD, neuroleptic-induced

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166
Q

Which etiologies cause chorea?

A

Huntington’s disease

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167
Q

What is chorea?

A

Variable steps, poor balance. movement disorder that causes involuntary, unpredictable body movements.

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168
Q

What is dystonia?

A

Involuntary posturing of the feet brought on by actions or intentions.

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169
Q

Which etiologies cause dystonia?

A

Cerebral palsy, birth injury, prenatal injury.

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170
Q

What is a diplegic gait?

A

Patients have involvement on both sides with spasticity in lower extremities worse than upper extremities. The patient walks with an abnormally narrow base, dragging both legs and scraping the toes. This gait is seen in bilateral periventricular lesions, such as those seen in cerebral palsy. There is also characteristic extreme tightness of hip adductors which can cause legs to cross the midline referred to as a scissors gait.

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171
Q

Which etiologies cause diplegic gait?

A

Cerebral palsy

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172
Q

Etiologies that cause hemiplegic gait?

A

This is clinically commonly seen in stroke patients. Also seen in any brain (e.g. brain injury, brain abscess, brain tumor, multiple sclerosis etc) lesion that results in upper motor neuron lesions.

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173
Q

What is cerebellar ataxia?

A

Patients can show dysmetria and intention tremor (only present during movement) on upper and lower limb testing (finger nose/heel shin). Ataxic gait

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174
Q

Etiologies that cause cerebellar ataxia?

A

Alcoholic cerebellar degeneration (midline), stroke, tumor, demyelination

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175
Q

What is defined as a cautious gait?

A

Most common ‘gait disorder’, adaptation to impairment, slower, short stride length, wide base – like walking on ice. Non-specific. May be associated with aging.

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176
Q

Clinical features of congenital cerebellar ataxias?

A

Early onset non-progressive ataxias associated with various syndromes as well as developmental abnormalities (e.g. Arnold-Chiari malformation, Dandy-Walker cysts)

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177
Q

Etiologies of acquired cerebellar ataxias?

A
  • Neurodegeneration: e.g. multiple system atrophy
  • Systemic: alcohol, celiac sprue, hypothyroidism, Wilson’s, thiamine deficiency, vitamin E deficiency
  • Toxins: carbon monoxide, heavy metals, lithium, anticonvulsants, solvents
  • Vascular: infarct, bleed, basilar migraine
  • Autoimmune: MS, Miller-Fischer (GBS)
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178
Q

Etiologies of hereditary autosomal recessive ataxia?

A

Friedrich’s ataxia, ataxia with oculomotor apraxia, ataxia telangiectasia, vitamin E deficiency

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179
Q

Signs of Friedrich’s ataxia?

A

Signs: gait and limb ataxia, weakness, areflexia, extensor plantar reflex, impaired proprioception and vibration, dysarthria

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180
Q

Most common hereditary autosomal dominant ataxia?

A

Most commonly spinocerebellar ataxias (SCAs); 30+ types, most commonly due to CAG repeats

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181
Q

Signs of hereditary autosomal dominant ataxia?

A

Ataxia and dysarthria, chorea, polyneuropathy, pyramidal and/or extrapyramidal features, dementia

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182
Q

Definition of syncope?

A

Syncope is a sudden transient self-limited loss of consciousness from global cerebral hypoperfusion with spontaneous recovery

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183
Q

Clinical features that differ seizure from syncope?

A

Preceding aura , tonic-clonic movements, tongue biting, urinary incontinence during episode, postictal state (confusion over 5 minutes after event vs return of consciousness with syncope)

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184
Q

Clinical features that differ stroke from syncope?

A

Weakness, numbness, visual changes, CN symptoms (diplopia, dysphasia, dysarthria) other focal neuro deficits, CVA risk factors (HTN, CAD, DM, DLD, Afib, obesity)

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185
Q

Clinical features that differ SAH from syncope?

A

Sudden onset, severe headache (thunderclap), nausea/vomiting, photophobia, CN palsy (III, IV)

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186
Q

DDx for syncope?

A

SYNCOPE

  • Neurally-mediated (reflex)
    • Situational
    • Vasovagal (most common)
    • Carotid sinus hypersensitivity
  • Neurogenic - vestibular stroke, seizures, autonomic insufficiency
  • Cardiogenic
    • Arrhythmia (brady, SVT, VT, AFib)
    • Valvular - aortic stenosis, mitral stenosis, pulmonary stenosis, tricuspid stenosis
    • Vascular - pulmonary hypertension, pulmonary embolism
    • Pericardial - tamponade
    • Myocardial - myocardial infarction, hypertrophic cardiomyopathy
  • Orthostatic – 30-20-10 (HR increases 30, SBP 20, DBP10)
    • Hypovolemia - acute blood loss, anemia, nausea/vomiting/diarrhea, inadequate intake. Presyncope/ syncope upon sitting/standing quickly
    • ANS dysfunction - focal neurological deficits (MS , MSA, PD, DM). Presyncope/ syncope upon sitting/standing quickly
    • Drugs - anti hypertensive (diuretics, nitrate, ACEi), rate slowing drugs (B blockers, digoxin, amiodarone), QTc-prolonging drugs (phenothiazine, quinidine, psych meds)
  • Psychogenic
  • Eating - hypoglycemic
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187
Q

Clinical features indicating a valvular etiology of syncope?

A

Sudden-onset syncope during exertion (HOCM) or when supine – may have CP, dyspnea, palpitations. FHx of sudden death, PMHx - HTN

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188
Q

Clinical features indicating a arrhythmic etiology of syncope?

A

Usually sudden and unprovoked (may have preceding palpitations). FHx of sudden death, PMHx - cardiac risk factors

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189
Q

Triggers of carotid sinus hypersensitivity

A

Triggers: head rotation/pressure on carotid sinus (shaving, tight collar)

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190
Q

Triggers of situational syncope?

A

Triggers: walking, defecation, micturition, prolong standing, after exercise, history similar events

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191
Q

Triggers of vasovagal syncope?

A

Triggers: Fear, heat, pain, stress, coughing, sneezing, GI stimulation/micturition (straining on BM or urine)

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192
Q

Investigations for syncope?

A
  • Labs: CBCd, lytes, Cr/urea, glucose, Mg, Ca, TSH
  • Imaging:
    • CT head – if clinically indicated (focal neuro deficits)
    • Echocardiogram – if clinically indicated (valvular heart disease evaluation)
    • CXR – if chest discomfort, SOB, crackles in lungs
  • Special Tests:
    • ECG
    • Carotid massage
    • EEG – seizures
    • 24h Holter
    • Cardiac enzymes – rule out ACS
    • Exercise stress test – if concerned about exercise-induced arrhythmia
    • Tilt table test – confirms vasovagal syncope
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193
Q

What is the San Francisco Syncope Rule?

A

Admit patient if they have 5 of any of the CHESS risk factors: CHF, Hematocrit<30, ECG Abnormalities, SBP<90mmHg, Shortness of Breath

194
Q

Treatment of vasovagal/situational syncope?

A

Lie down if pre syncope, adequate fluids and salt intake, SSRI (paroxetine 20 mg PO daily), vasoconstrictor (midodrine 2.5 10 mg PO TID), permanent cardiac pacing if recurrent , compression stockings

195
Q

Treatment of orthostatic syncope?

A

Gradual staged movements with postural changes, exercises, increase salt/fluid intake, elastic stockings, and minimize antihypertensive medication use. Medications include fludrocortisone 0.05 0.1 mg PO daily, midodrine, pseudoephedrine, ephedrine, DDAVP, and potentially pyridostigmine

196
Q

Etiology of Numbness/Tingling/Altered Sensation

A
  • CNS
    • Cortex/Thalamus,Brainstem
    • Spinal cord
  • PNS
    • Mononeuropathy
    • Radiculopathy
    • Polyneuropathy
    • Drugs: Chemotherapy, heavy metals, metronidazole
  • Psychogenic disorders – panic attacks, conversion disorder
  • Dermatological - herpes zoster, angioedema
197
Q

Cortex/Thalamus/Brainstem etiology for numbness/altered sensation?

A

Ischemic stroke, MS, inflammation, mass lesion (tumor, mets, abscess)

198
Q

Spinal cord etiology for numbness/altered sensation?

A

Trauma, compression (disc, tumor, mets, abscess), MS, infection (HIV, syphilis), cord infarction, vit B12 deficiency

199
Q

Mononeuropathy etiology for numbness/altered sensation?

A

Trigeminal neuralgia, carpal tunnel syndrome (median nerve), Saturday Night Palsy (radial nerve), ulnar nerve palsy, meralgia paresthetica, peroneal nere palsy

200
Q

Radiculopathy etiology for numbness/altered sensation?

A

Disc herniation, osteophytes, infections, epidural abscess, arachnoiditis, herpes zoster

201
Q

Polyneuropathy etiology for numbness/altered sensation?

A
  • DM, uremia, vasculitis, amyloidosis, hypothyroidism, Sjogren’s syndrome
  • Syphilis, HIV, lyme disease, EBV
  • EtOH, vit B12 deficiency, crticial illness polyneuropathy, GBS, paraneoplastic, hereditary neuropathies
202
Q

What are positive sensory symptoms?

A

Parasthesia/dysesthesia = tingling, pins and needles, prickling, burning, stabbing

203
Q

What are negative sensory symptoms?

A
  • Hypoesthesia – numbness, loss of sensation, analgesia, ataxia
  • Difficult to detect on exam (numbness, diminution/absence of feeling)
204
Q

There are 4 primary sensory modalities we test?

A

Vibration, proprioception, pain, and temperature

205
Q

Important questions to ask on history for numbness/tingling/altered sensation?

A
  • Quality, Timing, Migration, Progression
  • Distribution - focal, multifocal, unilateral or bilateral
  • Precipitating factors: recent trauma or injury, infection or illness, or occupational/environmental exposure, time of day, positional differences, anxiety provoking incidents that precede abnormal sensations
  • Associated symptoms: headache, weakness, rashes
  • PMHx: DM, stroke risk factors, Hx of autoimmune diseases, recent infections, malignancy
  • FHx - ask about childhood history of clumsiness or poor athletic performance, suggestive of hereditary cause
206
Q

Physical exam for numbness/tingling/altered sensation?

A
  • Inspection: gait, atrophy, fasciculations, signs of trauma/injury or vasculitic rashes (purpura, livedo reticularis)
  • Motor exam (strength and tone) – unilateral weakness (stroke)
  • DTR
  • Sensory exam: Differentiate between spinothalamic tract deficits (using light touch, sharp versus dull discrimination and temperature discrimination as necessary) and dorsal column deficits (using vibration and tests of proprioception)
  • Special tests: Compression test, Tinel’s test and Phalen’s maneuver. Straight leg raise and cross straight leg tests are indicated if sciatica is suspected
207
Q

Investigations for numbness/tingling/altered sensation?

A
  • Labs
    • CBCd, glucose, HbA1c
    • Vit B12, TSH, urea, Cr
    • Rheumatolgic (ANA, ANCA, RF, anti-SSA, anti-SSB, CRP)
    • Infectious screen (HIV, HepBsAg, HBV/HCV serology)
      • Toxin screen (heavy metals)
        • Malignancy screen (SPEP, UPEP)
  • Radiology/Imaging
    • Central lesions: MRI, MRA, CT, CTA
    • Spinal cord lesions: MRI of brainstem down to spinal sensory level
  • LMN lesions: EMG, nerve conduction studies, muscle/nerve bx
  • Lumbar puncture is myelitis is suspected
208
Q

What is mononeuropathy?

A

Focal lesion of individual nerve trunk, numbness/weakness in nerve territory, caused by compression/trauma/inflammation

209
Q

What is carpal tunnel syndrome?

A

Carpal tunnel syndrome is most common, caused by median nerve compression between carpal bones, flexor tendons, and carpal ligament

210
Q

What is cubital tunnel syndrome?

A

Cubital tunnel syndrome is second most common, caused by ulnar nerve entrapment at elbow

211
Q

What is polyneuropathy and its features?

A

Diffuse process that is dependent on length (often appears in longer nerves first) Stocking glove distribution. Symmetrical numbness, paresthesia. Associated with LMN findings – loss of reflex, weakness if motor nerve affected

212
Q

Etiology of axonal polyneuropathy?

A
  • Neoplastic - carcinoma, lymphoma, MGUS – IgA, IgG, IgM
  • Infectious - sepsis, HIV, Lyme
  • Metabolic - DM, uremia in chronic kidney disease
  • Vitamin deficiency – malabsorption
  • Drugs - cisplatin, taxanes, vincristine, isoniazid, nucleoside analogue
  • Inflammatory (disorders causing primary vasculitis - RA, Sjogren syndrome, polyarteritis nodosa)
213
Q

Etiology of demyelinating polyneuropathy?

A

Guillain-Barre + neoplastic + drugs (taxanes) + chronic inflammatory demyelinating polyneuropathy, hereditary neuropathies

214
Q

What is small fiber neuropathy?

A

Subtype of polyneuropathy with isolated involvement of small nerve fibers (pain and temp). Pain, burning, aching in the feet particularly at night. Preserved vibration/proprioception – dissociated sense loss

215
Q

How do you differentiate the site of median nerve injury?

A

If lesion is at carpal tunnel – LOAF muscles affected; if lesion at or above the elbow – may be lateral forearm wasting and the index finger held in extension (Benediction Sign)

216
Q

How do you differentiate the site of ulnar nerve injury?

A

Low lesion (below the wrist) characterized by marked hand clawing (because of unopposed flexor digitorum profundus flexion of DIPs) – high lesions have subtle clawing, termed ulnar paradox

217
Q

What is Saturday night palsy?

A

Compression of the radial nerve in the arm causing wrist drop with numbness on the back of the hand

218
Q

What is radiculopathy and its features?

A

Lesion of trunk of an individual nerve root compression (herniated disc, abscess, tumors). See change in sensation, weakness, atrophy in territory of individual nerve root distal to lesion site (dermatomal, myotomal territory – unilateral) + back/neck and limb pain +/- reflex loss.

219
Q

What is sensory neuronopathy and its features?

A

Degeneration of cell bodies in dorsal root ganglion. Affects all sensation – numbness, dysesthesia. Sensory ataxia, absent reflexes. Profound sensory loss is a hallmark of neuron sensory loss. NO MOTOR WEAKNESS. Very disabling than other neuropathies

220
Q

Etiology of sensory neuronopathy?

A
  • Often paraneoplastic – most common small cell lung cancer
  • Chemotherapeutic drugs, autoimmune
221
Q

What is a complete lesion of the spinal cord and its features?

A

Complete lesion of the spinal cord resulting in a sensory level (loss of sensations below the level of the lesion), paraplegia (paralysis of both legs) or quadriplegia with higher cervical lesions. Urinary incontinence/retention. LMN findings at the level of lesion and UMN findings below level of lesion

222
Q

What is a central cord lesion of the spinal cord and its features?

A

Lesions involve the crossing spinothalamic fibers usually in cervical cord. Loss of pain and temperature across the upper back, shoulders “Cape Distribution Sensory loss”, sacral sparing. With increasing size – weakness of hand muscles due to motor neurons in the anterior horn

223
Q

What is a Brown Sequard Syndrome (Hemi-Cord) and its features?

A

Diminished proprioception and vibration, on the side ipsilateral to the lesion. Decreased pinprick and temperature sensation on the contralateral side, weakness on ipsilateral side.

224
Q

What are the features of a brainstem lesion?

A
  • Ipsilateral CN weakness (facial droop, ptosis, dysarthria, dysphagia), contralateral body weakness: cerebellar ataxia, Horner’s syndrome.
  • Sensory deficit in the ipsilateral face and contralateral body. Crossed signs – face (ipsilateral), limbs (contralateral).
225
Q

What is Wallenberg Syndrome (Lateral Medullary Syndrome) and its features?

A

Loss of pain and temp in the ipsilateral face, contralateral body (spinothalamic), ipsilateral ataxia (cerebellar fibers), ipsilateral Horner’s Syndrome (sympathetics), dysphagia, hoarseness (IX, X), vomiting, vertigo (VII)

226
Q

What are the features of thalamus lesion?

A

Normal reflexes/tone; contralateral hemianesthesia, thalamic pain syndrome, contralateral homonymous hemianopsia, complex movement disorders, eye movements, can mimic cortical

227
Q

What is Thalamic Pain Syndrome?

A

Central post-stroke pain in the recovery phase of strokes. Sensory exam normal but severe pain + allodynia in contralateral hemibody

228
Q

What are the features of a cortical lesion?

A
  • Hyperreflexia, spasticity (velocity dependent), “A words” (aphasia: loss of acquired language, alexia: inability to read, agraphia: trouble writing, agnosia: inability to interpret sensations + recognize things, anosognosia: denial of neurological deficit, esp. paralysis, acalculia: inability to do simple math, astereognosis: cannot ID object by touch, agraphesthesia: cannot ID figures when written on skin); seizures, altered cognition, personality changes, hemiparesis (face > arm > leg MCA territory, leg > arm > face ACA), visual field defects (occipital lobe), neglect (esp. R parietal), memory loss
229
Q

Treatment of carpal tunnel syndrome?

A

Carpal tunnel syndrome is treated conservatively with night splints and glucocorticoid injections, oral glucocorticoids, surgical decompression

230
Q

Treatment of trigeminal neuralgia?

A

Carbamazepine, gabapentin, lamotrigine, microvascular decompression, rhizotomy

231
Q

Treatment of diabetic neuropathy?

A

Glycemic control; pain control; foot care; gabapentin, pregabalin, amitryptyline

232
Q

Treatment of radiculopathies?

A

Radiculopathies are managed pharmacologically with NSAIDs, analgesics, and muscle relaxants, or with physiotherapy and injections. Open discectomy/microdiscectomy

233
Q

Treatment of peripheral neuropathies?

A

Peripheral neuropathies are treated symptomatically with analgesia and anticonvulsants such as gabapentin and pregabalin. Tricyclic antidepressants and SNRIs may also be used. Transcutaneous electronic nerve stimulation (TENS) has been shown to be effective in some people.

234
Q

Clinical features of Guillain-Barre Syndrome (GBS)?

A
  • Fine paresthesias in toes and fingertips > weakness in lower/upper extremities (often ascending) > potential autonomic dysfunction (5%), cranial nerves, and respiratory involvementAscending glove and stocking distribution (sensory AND motor)
  • Ascending motor > sensory symptoms (but still get BOTH)
  • Areflexia: key feature (but preserved early on) + low/mid back pain
  • Check for predominant proximal and distal weakness and numbness suggesting polyradiculoneuropathy such as Guillain-Barre syndrome
235
Q

Precipitants of Guillain-Barre Syndrome (GBS)?

A

Campylobacter, CMV, URTIs, possibly flu shots

236
Q

Diagnosis of Guillain-Barre Syndrome (GBS)?

A

EMG (demyelinating neuropathy) + lumbar puncture (cytoalbuminergic dissociation = normal CSF WBC but increased CSF protein) + PFT (decreased FVC, MIP, MEP)

237
Q

Treatment of Guillain-Barre Syndrome (GBS)?

A

Plasmapheresis first then IVIG 0.5-1g/kg IV daily + ICU admission with respiratory support if FVC <20ml/kg or max inspiratory pressure <30 or max expiratory pressure <40 or rapid progression (<7 days) or autonomic involvement

238
Q

What is myasthenia gravis?

A

Autoimmune condition that targets acetylcholine receptors

239
Q

What are the symptoms of myasthenia gravis?

A

Dysphagia, diplopia, proximal muscle wasting, fatigable weakness

240
Q

What are the investigations for myasthenia gravis?

A

Acetyl choline receptor antibodies

241
Q

What is the treatment for myasthenia gravis?

A

IVIG, dexamethasone, severe plasmaphoresis

242
Q

Definition of a seizure?

A

Defined as the abnormal synchronized firing of electrical impulses in the brain causing a change in motor activity and/or behavior. Essentially, excitation of cortical neurons overcomes normal inhibition.

243
Q

What are potential seizure mimics?

A
  • Startle (Moro) reflex
  • GERD (Sandifer syndrome)
  • Breath-holding spells
  • Syncope
  • Psychogenic non-epileptic attacks (e.g. pseudoseizures)
  • Movement/tic disorders
  • Sleep disorders
  • Migraine variants
  • Myoclonic jerks secondary to brain injury - Lack of inhibition
244
Q

How to differentiate between seizure and syncope?

A

Syncope - Shaking after a LOC. Difference is that syncope has some dizziness and the LOC happens before the shaking. Seizure - movement starts before LOC. In syncope you don’t have a prolonged post-ictal confusion

245
Q

Classification of seizures?

A
  • Generalized
  • Focal/Partial
246
Q

What is a generalized tonic-clonic seizure?

A
  • Both hemispheres simultaneously, no aura, seizure may start with a scream then evolve into tonic (stiffening) and then clonic (twitching or jerking) activity. Lasts for 60-90s. Heavy breathing at the end, foaming at mouth, tongue biting and bladder incontinence. Loss of consciousness
  • May have prodrome of unease or irritability hours to days before
247
Q

What is defined as tonic and clonic?

A
  • Clonic: whole body repetitive rhythmic jerking movements
  • Tonic: whole body muscle rigidity in flexion or extension
248
Q

Generalized tonic-clonic seizure may occur alone or may be preceded by a partial seizure or an aura. When preceded by an aura, we may call this a _________.

A

Partial onset seizure with secondary generalization

249
Q

How do you bring about absence seziures in the clinic?

A

Hyperventilation

250
Q

What is the typical presentation of absence seizures and in what age group?

A

Generalized seizure that starts at 5-10yo but usually disappears as you get older. Starts abruptly without aura. Child may exhibit rapid eye blinking/fluttering – spacing out. 5-10s. Can be activated by hyperventilation! No aura or post-ictal fatigue/confusion.

251
Q

What are the clinical features of juvenile myoclonic epilepsy?

A
  • Myoclonic jerks – no preceding aura. Early morning myoclonus, Brief and bilateral but not always symmetric, Consciousness is preserved so patient aware of jerking movement
  • Triad of myoclonic jerk, generalized tonic-clonic seizure, absences
252
Q

What is an atonic seizure

A

Is a brief loss of muscle tone, lasting only a few seconds that may cause injury for instance if the patient falls, or the head drops unexpectedly. If the patient falls, this is commonly referred to as a “drop attack”.

253
Q

What is a complex focal/partial seizure?

A
  • Arising from an area of a brain then spreads
  • Patient may appear to be awake but with impairment of awareness (not LOC)
254
Q

What is a simple focal/partial seizure?

A
  • Can arise from any area of the brain (focal or lateral), no LOC/intact awareness
255
Q

What should be asked on the pre-ictal history for a seizure?

A
  • Aura: Happens right before a seizure starts (seconds) – déjà vu, jamais vu, vision problems, dizziness, odd smells, sounds, headache, nausea
  • Prodrome (hours to days before): changes in mood, sleep changes, anxiety, problems with focus
  • Preceding Events: sitting still vs. going to the bathroom - urination/defecation ~ vasovagal syncope
  • Preceding Symptoms: sweating + light-headedness + nausea - ~ syncope
  • Trigger: head injury + strenuous physical exercise (arrhythmia) + preceding illness (febrile seizure)
256
Q

What should be asked on the ictal history for a seizure?

A
  • Motor Symptoms: repetitive non-purposeful movements + staring + lip-smacking + fainting + stiffening of extremities + rhythmic shaking of extremities + unilateral or bilateral
  • Autonomic/Sensory Symptoms: nausea + feeling odd/peculiar + bowel/bladder control loss + numbness + tingling + odd smells or sounds + any change in skin color (cyanosis ~ seizure) + drooling + vomiting + tongue biting (~seizure)
  • Responsiveness: during spell + eyes open/closed + eyes attending to environment vs. fixed
    • Most seizure activity cannot be interrupted with verbal/physical stimulation
  • Duration: <30 seconds more likely syncope, >30 seconds more likely seizure
257
Q

What are the features of non-epileptic seizures?

A

Awareness during ictal phase + eye fluttering + bystanders can modulate symptoms intensity + pelvic thrusting + slow onset + non-rhythmic + closed eyes + no post-ictal confusion + situation dependent

258
Q

What should be asked on the post-ictal history for a seizure?

A

Post-event amnesia/confusion/lethargy/tiredness + headaches + muscle aches + transient focal weakness of one side (Todd’s Paresis) + nausea + vomiting + how long until back to baseline

259
Q

______ or _______ do not have post-ictal confusion (normal EEG + normal MRI; they look like panic attacks)

A

Absence or frontal lobe seizures

260
Q

What is the physical exam for seizures?

A
  • Vitals (sinus rhythm? HR? Orthostatic hypotension? Mental status?)
  • Always Examine for: meningismus + signs of systemic illness + toxidromes + tongue biting
  • Neurological Exam
  • Cardiac Exam
261
Q

Investigations for seizures?

A
  • Blood Work
    • CBC, lytes, Na, Ca, glucose, troponin, urea
    • CK, TSH, INR, AST, ALT, bilirubin, ALP, b-HCG, tox screen
    • Prolactin
  • Imaging
    • Emergency non-contrast CT if significantly aLOC + new focal deficit + no return to baseline
    • MRI
  • Special Tests:
    • EEG as outpatient to get license back - Don’t need to repeat this if history of seizures; sleep deprived EEG best
    • Do drug level if seizure and S/E
    • LP (if suspect meningitis/encephalitis)
262
Q

Indications for MRI for seizures?

A

<1yo + significant acute cognitive/motor impairment + unexplained abnormal neuro exam + focal onset seizure without generalization + abnormal focal EEG

263
Q

After how many occurences do you typically start treating someone for a seizure?

A

After 2nd seizure or if high risk for recurrent seizures then treat after first

264
Q

What are the anticonvulsants used for partial seizures?

A
  • Under 2: Phenobarbital, Levitiracetam (Keppra)
  • Over 2: Carbamazepine, Lamotrigine
265
Q

What are the anticonvulsants used for generalized tonic-clonic seizures?

A
  • Under 2: Phenobarbital, Levitiracetam
  • Over 2: Valproate, Topiramate, Carbamazepine
266
Q

What is the anticonvulsant used for absence seizures?

A

Ethosuximide (Zarontin)

267
Q

What are the anticonvulsants used for atonic/myoclonic seizures?

A

Valproate

268
Q

What are the anticonvulsants used for atonic seizures?

A

Valproic Acid (Depakene/Epival) or Phenobarbital

269
Q

What is the risk of having another seizure after your first episode?

A

Risk of second seizure is 30-50%, then after second seizure risk of next one is >80%

270
Q

What are the precautions one should take after first episode of seizures?

A

Take precautions with fire, water, heights, and roads + no driving until cleared by physician (no driving after 3 months, and must be seizure free for 6 months)

271
Q

What is a breath holding spell?

A

Benign paroxysmal disorder occurring in healthy children usually provoked by emotional upset or minor injury - unintentional involuntary reflex

272
Q

Clinical features for breath holding spell?

A
  • 6m – 6y; breath holding progressing to cyanosis or syncope
  • There is an antecedent event, heart rate decreases and the child becomes pale, and there is NO post-ictal period.
273
Q

What are the two types of breath holding spells?

A

Two types are cyanotic (see facial cyanosis), and pallid (child becomes very pale) - soon thereafter infant regains consciousness and breathes normally.

274
Q

Investigation + management for breath holding spells?

A

Investigations/Management: ECG for first spell to rule out prolonged QT - reassurance, sometimes blowing air forcefully on face will terminate episode early

275
Q

What is the clinical presentation for BECRS?

A

Benign childhood epilepsy with centrotemporal spikes (often first thing in the morning, awakes them from sleep); self-limited/benign (between 5-10 years) – often see single nocturnal seizure with clonic movement of the mouth accompanied by gurgling sounds (seizures usually resolve by 16 years old) and may be associated with migraine

Start in face (drooling) and then move into arm and then leg. As it moves to legs, consciousness is not preserved

276
Q

What are the clinical features of benign sleep myoclonus?

A

Usually eyes are closed/rolled upwards + kids/babies are sleeping + notice motor ‘twitch’

277
Q

What is a simple febrile seizure?

A

Precipitated by fever + normal development + no focal neurologic deficits after the seizure + 1 in 24hrs + generalized + <15m + <5y old = simple febrile seizure. If not, then “complex” and higher risk of recurrence

278
Q

What are the investigations + management of febrile seizures?

A

No diagnostic testing needed - if still seizing can give IV lorazepam or midazolam + reassurance that they are harmless and do not cause brain damage; if 5+ febrile seizures = you have epilepsy - note that antipyretics don’t prevent febrile seizures

279
Q

What is the presentation of status epilepticus?

A

>5 minutes of continuous seizure activity or 2+ seizures without returning to baseline mental status - usually generalized tonic-clonic

280
Q

Stat investigations for status epilepticus?

A

ABG + CBCd + lytes + extended lytes (Mg/Ca/Po) + Cr + glucose + toxic screen + antiepileptic drug level

281
Q

Management of status epilepticus?

A
  • ABCs + O2 + establish IV + monitors
  • If Hypoglycemia: thiamine 100mg IV + 50% dextrose 50ml IV
  • First Line: lorazepam 2mg q1-3min IV push or rectal diazepam if no IV access
  • Second Line: phenytoin 20mg/kg IV, no faster than 50mg/min – start continuous monitor
  • Note: give benzos and phenytoin in DIFFERENT IVs – they precipitate
282
Q

Etiology of seizures?

A

Alcohol and illicit drug use/withdrawal, brain injury/abnormality (tumour, trauma, vascular), CNS infection, fever (children), metabolic (hypoglycemia, electrolyte abnormalities, liver/renal failure), medications - bupropion, theophylline, isoniazide, imipenem, high dose penicillin, meperidine, or be a genetic or inherited cause

283
Q

Diagnostic criteria for epilepsy?

A

Any of 1/3 criteria - => 2 unprovoked seizures >24h apart; 1 unprovoked seizure with probable seizure ->60% over next 10 years (e.g. a structural lesion associated with high risk of recurrence)

284
Q

Etiology of epilepsy?

A

Genetic, structural (e.g. prior stroke, tumour, meningo/encephalitis, perinatal insult, vascular malformation, malformation of cortical development, neurodegenerative disorders), or unknown

285
Q

Tonic posturing from gut content coming into the esophagus

A

Sandifer syndrome

286
Q

What does the post-ictal phase look like in generalized tonic-clonic seizure?

A

Post-ictal phase: flaccid limbs, extensor plantar reflexes, headache, confusion, aching muscles, sore tongue, amnesia, elevated serum CK lasting hours; may have focal paralysis (Todd’s paralysis)

287
Q

What are the precipitates of juvenile myoclonic epilepsy?

A

Seizures are precipitated by sleep deprivation, alcohol ingestion, flickering light and awakening from sleep

288
Q

What are the types of generalized seizures?

A
  • Clonic
  • Tonic
  • Tonic-clonic (grand mal)
  • Absence
  • Myoclonic
  • Atonic
289
Q

Motor symptoms of focal with intact awareness (simple partial) seizure?

A

Dystonic posturing, clonic movements, forceful turning of eyes and/or head, focal muscle rigidity/jerking ± Jacksonian march (spreading to adjacent muscle groups)

290
Q

Sensory symptoms of focal with intact awareness (simple partial) seizure?

A

Unusual sensations affecting vision, hearing, smell, taste, or touch

291
Q

Autonomic symptoms of focal with intact awareness (simple partial) seizure?

A

Epigastric discomfort, pallor, sweating, flushing, piloerection, pupillary dilatation

292
Q

Classic complex seizure is characterized by ____ such as chewing, swallowing, lip-smacking, scratching, fumbling, running, disrobing, and other stereotypic movements

A

Automatisms

293
Q

What is a secondarily generalized seizure?

A

Focal seizures that spread and involve the 2 hemispheres. Looks like tonic-clonic seizure

294
Q

Management of acute seizure control?

A
  • Benzodiazepines: lorazepam 1mg IV/SL PRN up to a total dose of 0.1mg/kg or diazepam 10mg PO q6h and 5mg PO q2h PRN
  • Antiepileptic: fosphenytoin 20mg/kg IV or phenytoin 300mg IV over 10 min or phenobarbital, carbamazepine, valproate
  • If EtOH Withdrawal: add thiamine 100mg IV/PO daily + multivitamin 1 tab IV/PO daily + folate
295
Q

What is a simple febrile seizure?

A

Most common, must be generalized, <15 minutes and must not recur within a 24 hr period. Must have a normal developmental history, no evidence of CNS infection and usually a FHx of febrile seizures

296
Q

What is a complex febrile seizure?

A

Either focal, prolonged or recurs within 24 hour. Indicates more serious underlying etiology such as encephalitis, meningitis, or an underlying seizure disorder.

297
Q

Clinical presentation of temporal lobe seizures?

A

Motionless stare at onset, aura (fear/anxiety, deja-vu, odd smell, rising epigastric sensation), automatisms (lip-smacking, or gestures). Duration is 30-120seconds. May have secondary generalization

298
Q

Clinical presentation of frontal lobe seizures?

A

Abrupt onset, prominent motor and complex gestural automatisms , forced vocalization, secondary generalization is COMMON as is nocturnal concurrence. Rapid recovery. Can be misdiagnosed as pseudoseizures.

299
Q

Clinical presentation of occipital lobe seizures?

A

Simple partial onset, decreased vison, forced blinking, ocular flutter. Contralateral head/eye deviation, secondary generalization.

300
Q

DDx of objective muscle weakness?

A
  • Generalized
    • Myopathy (proximal > distal weakness)
      • endocrine: hypothyroidism, hyperthyroidism, Cushing’s syndrome
      • rheumatologic: polymyositis, vasculitis
      • infectious: HIV, influenza
      • other: collagen vascular disorders, steroids, statins, alcohol, electrolyte disorders
    • NMJ (MG, botulism, LEMS, organophosphate poisoning)
    • Cachexia
  • Localized
    • UMN (vasculitis, abscess, brain tumour, vitamin B12 deficiency, MS, stroke)
    • radicular pain (i.e. nerve root)
    • anterior horn cell (spinal muscular atrophy, ALS, polio, paraneoplastic)
    • peripheral neuropathy (peroneal muscle atrophy, GBS, leprosy, amyloid, myeloma, DM, lead toxicity)
301
Q

DDx of asthenia?

A
  • Chronic illness (cardiac, pulmonary, anemia, infection, malignancy)
  • Depression, deconditioning
302
Q

What is the MRC Scale – Muscle Strength?

A
  • 0 - no contraction
  • 1 - flicker of contraction – no movement
  • 2 - active movement with gravity eliminated
  • 3 - active movement against gravity
  • 4 - active movement against gravity and resistance (4-, 4, 4+)
  • 5 - normal power
303
Q

UMN lesion findings?

A

Normal bulk, spastic/hypertonicity, weakness, upper extremity flexors stronger, lower extremity extensors stronger→ pyramidal position, hyperreflexia, babinski +, contralateral pronator drift, positive forearm rolling + finger tapping tests

304
Q

What is spasticity?

A

^resistance to passive displacement across a joint, velocity dependent

305
Q

LMN lesion findings?

A

Atrophy, fasciculations, flaccid/normal tone, hypo/areflexia, plantar responses down-going, +/-sensory distortion

306
Q

Clinical features of mononeuropathy multiplex?

A

Note change in sensation, weakness, atrophy in territories of several individual nerves distal to lesion site +/- reflex loss +/- autonomic changes

307
Q

What typically causes mononeuropathy multiplex?

A

Suggests systemic process. Usually due to vasculitis. Lesions of trunks of several individual nerves (not at usual sites of entrapment/compression) – ischemia secondary to vasculitis

308
Q

Clinical features of myopathies?

A

Proximal, symmetric muscle weakness (hips/shoulders→ trendelenburg gait) +/-tenderness, atrophy, hyporeflexia, increased CK→ necrosis; more likely chronic/insidious, no sensory Sx, pain related to disability, respiratory + swallowing usually later/absent

309
Q

Etiology of myotonic dystrophy?

A

Chronic/progressive, autosomal dominant (50% inheritance risk, trinucleotide repeat, DMPK gene, variability with age of onset

310
Q

Clinical features of myotonic dystrophy?

A

Appearance: ptosis, bifacial weakness, frontal baldness (including women), triangular face giving a drooping/dull appearance

311
Q

Physical exam findings of myotonic dystrophy?

A
  • Distribution of weakness: distal weaker than proximal (in contrast to other myopathies), steppage gait
  • Myotonia: delayed relaxation of muscles after exertion (elicit by tapping on thenar muscles with hammer)
  • Cardiac: 90% have conduction defects (1o heart block; atrial arrhythmias)
  • Respiratory: hypoventilation 2o to muscle weakness
  • Ocular: subcapsular cataracts, retinal degeneration, decreased intraocular pressure
  • Other: DM, infertility, testicular atrophy
  • EMG: subclinical myotonia - long runs with declining frequency and amplitude
312
Q

Treatment of myotonic dystrophy?

A
  • Management of myotonia: phenytoin
  • Genetic counselling, monitor cardiac, respiratory, swallowing function; supportive therapies
313
Q

Clinical features of neuromuscular junction disorders?

A

Fluctuating weakness (fatiguability), usually oculobulbar first (diplopia, lid droop – ptosis, dysarthria, dysphagia, drooling), or generalized to muscles of respiration. No pain, no change in sensation, and no alteration in stretch reflexes or presence of increased CK or atrophy.

314
Q

What is myasthenia gravis?

A

Autoimmune condition due to anti-Ach or anti-muscle specific kinase antibodies, resulting in early saturation at the NMJ and inadequate muscle activation with increasing nerve stimulation

315
Q

Clinical features of myasthenia gravis?

A
  • Fatigable, symmetric, or asymmetric weakness without reflex changes, sensory changes, or coordination abnormalities
  • Ocular (diplopia/ptosis), bulbar (dysarthria/dysphagia), and/or proximal limb weakness
  • Symptoms may be exacerbated by infection, pregnancy, menses, and various drugs
  • Respiratory muscle weakness may lead to respiratory failure
316
Q

Investigations for myasthenia gravis?

A

Clinical Dx, ice pack test (ocular signs reverse with cooling), edrophonium test (tensilon test): reduces muscle weakness by blocking acetylcholinesterase enzymes prolonging ACh in synaptic cleft, anti-ACh R antibodies

317
Q

Treatment for myasthenia gravis?

A
  • First line treatment: anticholinesterase drugs (pyridostigmine)
  • Corticosteroids (e.g.prednisone): If acetylcholinesterase inhibitors not effective
  • Immunosuppression (e.g. azathioprine, cyclophosphamide, mycophenolate): can be used as steroid-sparing therapy
  • Short-term immunomodulation (e.g. IVIG and plasma pheresis): for crisis
  • Thymectomy: option in non-thymomatous MG; 85% remission rate
318
Q

Hallmark symptom of nerve root/radiculopathy?

A

Hallmark symptom is intermittent pain and numbness in feet/legs while walking from narrowing of the spinal cord “neurogenic claudication”

319
Q

Clinical features of motor neuron disease?

A

Disease affecting motor neurons diffusely (infectious – poliomyelitis / degenerative – ALS). Weakness if bilateral but often asymmetric; bulbar – dysarthria, dysphagia (but NOT oculomotor), atrophy, and fasciculations. No change in sensation.

320
Q

Definition of Amyotrophic Lateral Sclerosis (ALS)?

A

Progressive neurodegenerative disease that causes UMN and LMN symptoms and is ultimately fatal

321
Q

Clinical features of ALS?

A
  • Limb motor symptoms: segmental and asymmetrical UMN and LMN symptoms
  • Bulbar findings: dysarthria (flaccid or spastic), dysphagia, tongue atrophy and fasciculations, facial weakness and atrophy
  • Pseudobulbar affect, frontotemporal dementia (up to 10%)
  • Sparing of sensation, ocular muscles, bowel, bladder, sphincters
  • Swallowing failure = aspiration. Respiratory muscle weakness = ventilator failure.
322
Q

Treatment of ALS?

A
  • Riluzole
  • Symptomatic relief
    • Spasticity/cramping: baclofen, tizanidine, regular exercise, and physical therapy
    • Sialorrhea: TCA (i.e. amitriptyline), sublingual atropine drops, parotid/submandibular Botox (rare)
    • Pseudobulbar affect: dextromethorphan/quinidine, TCA, SSRI
  • Non-pharmacologic: high caloric diet, ventilatory support (especially BiPAP), early nutritional support (i.e. percutaneous endoscopic gastrostomy tube), rehabilitation (PT, OT, SLP), psychosocial support
323
Q

Etiology of dorsal column lesion?

A

Vit B12 deficiency, syphilis, specific stroke/MS lesion, vit E. deficiency

324
Q

Etiology of generalized pain disorders?

A
  • Fibromyalgia/Chronic fatigue syndrome
  • Polymyalgia rheumatica (PMR)
  • Mental health disorders (e.g., depression, somatic symptom disorders)
325
Q

Epidemiology of polymyalgia rheumatica (PMR)?

A

Age of onset typically >50yr, F:M=2:1

326
Q

Signs and symptoms of polymyalgia rheumatica (PMR)?

A
  • Constitutional symptoms prominent (fever, weight loss, malaise)
  • Pain and stiffness of symmetrical proximal muscles (neck, shoulder and hip girdles, thighs)
    • Shoulder symptoms reflect proximal bursitis (eg, subdeltoid, subacromial) and less often bicipital tenosynovitis or joint synovitis.
  • Gel phenomenon (stiffness after prolonged inactivity) - Stiffness in the morning is typical and lasts > 60 minutes.
327
Q

Physical exam findings of polymyalgia rheumatica (PMR)?

A

Physical exam reveals tender muscles, but no true weakness or atrophy

328
Q

Investigations for polymyalgia rheumatica (PMR)?

A

Often shows anemia of chronic disease, elevated platelets, elevated ESR and CRP, and normal CK; up to 5% of PMR reported with normal inflammatory markers

329
Q

Treatment for polymyalgia rheumatica (PMR)?

A

Start with low prednisone dose of 15- 20mg PO OD, reconsider diagnosis if no response within several days

Taper slowly over 1yr period with closely monitoring

Relapses should be diagnosed and treated on clinical basis; do not treat a rise in ESR as a relapse

Monitor for steroid side effects, glucocorticoid-induced osteoporosis prevention, and follow for symptoms of GCA

330
Q

Clinical features of temporal arteritis?

A
  • Abrupt monocular loss of vision, pain over the temporal artery, jaw claudication, scalp tenderness,
  • Constitutional symptoms, and PMHx of polymyalgia rheumatica
  • Ischemic optic atrophy
  • 50% lose vision in contralateral eye if untreated
331
Q

Epidemiology of temporal arteritis?

A

More common in women >60yr

332
Q

Diagnosis of temporal arteritis?

A
  • Temporal artery biopsy + increased ESR and CRP (ESR can be normal, but likely 80-100 in first hour)
  • If biopsy is negative, biopsy contralateral side
333
Q

Treatment of temporal arteritis?

A
  • High dose corticosteroids (12mos) [no other immunosuppressants allow steroid sparing!], calcium/vit D/bisphosphonates, low dose ASA to prevent strokes
  • If diagnosis of GCA is suspected clinically: start STAT treatment + perform temporal artery biopsy to confirm diagnosis within 2 wk of initial presentation
334
Q

Definition of fibromyalgia?

A

Chronic (>3mo), widespread (axial, left-and right-sided, upper and lower segment), non-articular pain with characteristic tender points

335
Q

Diagnostic criteria for fibromyalgia?

A

A patient satisfies diagnostic criteria for fibromyalgia if the following 3 conditions are met:

  1. Widespread Pain Index (WPI) ≥7 and Symptom Severity (SS) scale score ≥5 or WPI 3–6 and SS scale score ≥9
  2. Symptoms have been present at a similar level for at least 3 mo
  3. The patient does not have a disorder that would otherwise explain the pain
336
Q

Epidemiology of fibromyalgia?

A
  • F:M=3:1
  • Primarily ages 25-45yr, some adolescents
  • Overlaps with chronic fatigue syndrome and myofascial pain syndrome
  • Strong association with psychiatric illness
337
Q

Signs and symptoms of fibromyalgia?

A
  • Wide spread aching, stiffness
  • Easy fatigability
  • Sleep disturbance: non-restorative sleep, difficulty falling asleep, and frequent wakening
  • Symptoms aggravated by physical activity, poor sleep, emotional stress
  • Patient feels that joints are diffusely swollen although joint examination is normal
  • Neurologic symptoms of hyperalgesia, paresthesias, allodynia
  • Associated with irritable bowel or bladder syndrome, migraines, tensionH/As, restless leg syndrome, obesity, depression, and anxiety
338
Q

Physical exam findings of fibromyalgia?

A

Should reveal only tenderness with palpation of soft tissues, with no specificity for trigger/tender points

339
Q

Investigations for fibromyalgia?

A
  • Blood work: includes TSH and ESR; all typically normal unless unrelated, underlying illness present
  • Serology: do not order ANA or RF unless there is clinical suspicion for a connective tissue disease
  • Laboratory sleep assessment
340
Q

Non-pharmacological therapy for fibromyalgia?

A
  • Education
  • Exercise program (walking, aquatic exercises), physical therapy (good posture, stretching, muscle strengthening, massage)
  • Stress reduction, CBT
  • No evidence for alternative medicine such as biofeedback, meditation, acupuncture
341
Q

Pharmacological therapy for fibromyalgia?

A
  • low dose tricyclic antidepressant (e.g. amitriptyline)
    • for sleep restoration
    • select those with lower anticholinergic side effects
  • SNRI: duloxetine, milnacipran
  • anticonvulsant: pregabalin, gabapentin
  • analgesics may be beneficial for pain that interferes with sleep (NSAIDs, not narcotics)
342
Q

What is nocieptive pain?

A

Nociceptive pain is due to chemical, thermal, and/or mechanical damage activating nociceptors and inflammatory response.

343
Q

What is neuropathic pain?

A

Neuropathic pain is caused by damage to or disorders of the central or peripheral nervous system that results in pain perception without actual tissue injury.

344
Q

What is spontaneous pain?

A

Unprovoked burning, shooting, or lancinating pain

345
Q

What is parasthesia?

A

Spontaneous abnormal non-painful sensation (e.g. tingling)

346
Q

What is dysesthesia?

A

Evoked pain with inappropriate quality or excessive quantity

347
Q

What is allodynia?

A

A dysesthetic response to a non-noxious stimulus

348
Q

What is hyperalgesia?

A

An exaggerated pain response to anoxious stimulus

349
Q

Side effects of opioids?

A

Nausea, drowsiness (No driving at all on initiation or adjustment of opioids because of drowsiness), pruritis, constipation (Everyone gets constipated and this never goes away - Need to also give them a laxative), addiction, pseudo-addiction, withdrawal, tolerance, opioid induced neurotoxicity

350
Q

WHO opioid ladder?

A
  • Step 1: non-opioids (acetaminophen or NSAID)
  • Step 2: weak opioids - codeine and tramadol. These both also have ceiling effects at certain daily doses. Tramadol can be serotonergic so be mindful of serotonin syndrome
  • Step 3: strong opioids - oxycodone, methadone, hydromorphone, morphine. Sometimes you can go directly to step 3 if you’re sure that’s the appropriate first thing to try
351
Q

Clinical features of opioid induced neurotoxicity?

A

Vivid dream, hallucinations, myoclonus, confusion, hyperalgesia

352
Q

Treatment of opioid induced neurotoxicity?

A

Goal is to catch it early, screen everyone for these symptoms. Hydration, decrease/rotate opioid, educate patient/caregivers, usually takes 3-4 days for metabolites to clear

353
Q

What should be the breakthrough dose

A

10% of total daily dose

354
Q

If patient is using > 3 BTA/day will need to titrate

A
  • Add up BTA + ATC = total 24 hr dose; divide by 6 for new q4h dosing schedule
  • Increase ATC dosing by 20-30% (to nearest tablets that are possible)
355
Q

Pharmacologic adjuvants for bone pain?

A

Corticosteroids (Usually use dexamethasone for the corticosteroid), bisphosphonates

356
Q

Pharmacologic adjuvants for neuropathic pain?

A

Antidepressants (Duloxetine), corticosteroids, anticonvulsants (gabapentin much cheaper than pregabalin, carbamazepine)

357
Q

Non-Pharmacological adjuvants for pain?

A
  • Physical (PT, acupuncture, chiropractic manipulation, massage)
  • Psychoeducational (CBT, family therapy, education, psychotherapy)
358
Q

Symptoms and signs of neuropathic pain?

A
  • Hyperalgesia, allodynia
  • Subjectively described as burning, heat/cold, pricking, electric shock, perception of swelling, numbness
  • Can be spontaneous or stimulus evoked, distribution may not fall along classical neuro-anatomical lines
  • Associated issues: sleep difficulty, anxiety/stress/mood alteration
359
Q

Causes of neuropathic pain?

A
  • Sympathetic: CRPS
  • Non-sympathetic: damage to peripheral nerves
    • Systemic disease: DM, thyroid disease, renal disease, rheumatoid arthritis, multiple sclerosis
    • Nutritional/toxicity: alcoholism, pernicious anemia, chemotherapy
    • Infectious: post-herpetic, HIV
    • Trauma/compression: nerve entrapment, trigeminal neuralgia, post-surgical, nerve injury, cervical/lumbar radiculopathy, plexopathy
  • Central: abnormal CNS activity
    • Phantom limb, post spinal cord injury, post stroke, MS
360
Q

Pharmacotherapy treatment for neuropathic pain?

A

Stepwise approach (Canadian Pain Society, 2014)

  • 1st line: gabapentinoids, TCA, SNRI
  • 2nd line: tramadol, opioid analgesics
  • 3rd line: cannabinoids
  • 4th line: topical lidocaine (second line for postherpetic neuralgia), methadone, lamotrigine, lacosamide, tapentadol, botulinum toxin
361
Q

Non-pharmacologic treatment for neuropathic pain?

A
  • Neuropsychiatry: CBT, psychotherapy
  • Rehabilitation: physiotherapy
362
Q

Surgical treatment for neuropathic pain?

A

Dorsal column neurostimulator, DBS (thalamus)

363
Q

Clinical features of trigeminal neuralgia?

A
  • Recurrent episodes of sudden onset, severe, excruciating, unilateral, paroxysmal, shooting “electric” pain in trigeminal root territory (V3>V2>>V1)
  • May have normal sensory exam
  • Pain lasts seconds/minutes over days/weeks; may remit for weeks/months
364
Q

Triggers of trigeminal neuralgia?

A

Triggers: touching face, eating, talking, cold wind, shaving, applying make-up

365
Q

Etiology of trigeminal neuralgia?

A
  • Classic TN: compression of CN V by tortuous blood vessel (usually superior cerebellar artery)
  • 2o TN: cerebellopontine angle tumour (5%), MS (5%)
  • Idiopathic TN
366
Q

Epidemiology of trigeminal neuralgia?

A
367
Q

Diagnosis of trigeminal neuralgia?

A
  • Clinical diagnosis
  • Investigate for secondary causes, which are more likely if bilateral TN or associated sensory loss
    • MRI to rule out structural lesion, MS, or vascular lesion
368
Q

Treatment of trigeminal neuralgia?

A
  • First line: carbamazepine or oxcarbazepine
  • Second line: baclofen or lamotrigine
  • For medically-refractory classic TN, consider microvascular decompression
  • Neurosurgical options for medically-refractory TN: trigeminal ganglion percutaneous technique, gamma knife radiosurgery, invasive percutaneous denervation (radiofrequency/glycerol), percutaneous balloon microcompression, microvascular decompression
  • Narcotics not generally recommended
369
Q

Clinical features of postherpetic neuralgia?

A
  • Pain persisting in the region of a cutaneous outbreak of herpe szoster
  • Constant deep ache or burning, intermittent spontaneous lancinating/jabbing pain, allodynia
  • Distribution: thoracic, trigeminal, cervical, lumbar, sacral
  • Associated symptoms: impaired sleep, decreased appetite, decreased libido
370
Q

Prevention of postherpetic neuralgia?

A
  • Varicella zoster vaccine (Varivax) in childhood reduces incidence of varicella zoster
  • Herpes zoster vaccine (Zostavax or Shingrix) reduces incidences of shingles, PHN, and other herpetic sequelae
  • Zostavax is a live vaccine, recommended for patients >60 yr old
  • Shingrix is a recombinant vaccine, recommended for patients >50 yr old (more efficacious than Zostavax)
371
Q

Etiology and pathogenesis of postherpetic neuralgia?

A

Destruction of the sensory ganglion neurons (e.g. dorsal root, trigeminal, or geniculate ganglia) secondary to reactivation of herpes zoster infection

372
Q

Treatment of postherpetic neuralgia?

A
  • Medical: TCA (e.g. amitriptyline), anti-convulsants (e.g. pregabalin, gabapentin), analgesia (e.g. opiates, lidocaine patch), intrathecal methylprednisolone, topical capsaicin
    • Early treatment of acute herpes zoster with antivirals (longer-acting famciclovir and valacyclovir more effective)
    • Treatment of herpes zoster with corticosteroids DOES NOT decrease PHN
  • Surgical: spinal tractotomy, dorsal root entry zone lesion, DBS of thalamus
373
Q

All the elbow flexors in the arm are from which nerve root?

A

C5,C6

374
Q

Three common groups that share C5,C6?

A

Deltoid (axillary n), Biceps (musculocutaneous n), Brachioradialis (radial n)

375
Q

Elbow extensors are primarily which nerve roots?

A

C7 but also has some C8 and occasionally C6

376
Q

Pronator teres and suppinator (opposing muscle actions) are both which nerve roots?

A

C6, C7

377
Q

All intrinsic muscles in the hand are from which nerve roots?

A

C8, T1

378
Q

Femoral nerve and obturator nerve share the same nerve roots

A

L2, L3, L4

379
Q

Tibialis anterior and tibialis posterior share the same root?

A

L4, L5

380
Q

Ankle evertors (peroneus longus and brevis) have which nerve roots?

A

L5, S1

381
Q

Gluteus maximus has which nerve roots?

A

L5, S1, S2

382
Q

Gluteus medius/minimus have which nerve roots?

A

L4, L5, S1

383
Q

Sciatic nerve in the back of the thigh (ie.Hamstrings) is from which nerve roots?

A

S1, S2

384
Q

All intrinsic muscles of the foot are from which nerve roots?

A

S1, S2

385
Q

Tibial nerve in the back of the leg (Gastrocnemius, Soleus, & Toe flexors with the exception of the Tibialis post.) are from which nerve roots?

A

S1, S2

386
Q

Mechanism of peripheral nerve injury

A
  • Ischemia
  • Nerve entrapment – nerve compressed by nearby anatomic structures, often secondary to localized, repetitive mechanical trauma with additional vascular injury to nerve
  • Direct trauma (e.g. transection, laceration, contusion)
  • Iatrogenic
387
Q

Two pathological processes of nerve damage?

A
  • Demyelination: damage to myelin sheath.
  • Wallerian degeneration: axonal damage leading to degeneration of the nerve distal to injury but not proximally, makes sense because if you damage upstream, downstream is messed.
388
Q

Investigations for peripheral nerve injury?

A
  • Electrophysiological studies: EMG/nerve conduction study (assess nerve integrity and monitoring recovery after 2-3 wk post-injury)
  • Labs: blood work (e.g. CBC, TSH, Vitamin B12), CSF
  • Imaging: C-spine, chest/bone x-rays, myelogram, CT, magnetic resonance neurography, angiogram if vascular damage is suspected
389
Q

Clinical exam for peripheral nerve injuries?

A

Clinical exam: muscle bulk and tone, power, sensation, reflexes, localization via Tinel’s sign (paresthesias elicited by tapping along the course of a nerve)

390
Q

Classification of peripheral nerve injuries?

A
  • Neurapraxia (class I)
  • Axonotmesis (class II)
  • Neurotmesis (class III)
391
Q

What is neuropraxia?

A

Axon structurally intact but fails to function. Though we have some demyelination there is no axonal damage and so we do not have Wallerian degeneration (part of axon separates distal to cell body). Demyelination – reduced conduction velocity. Neuropraxia affects thick myelinated fibres usually and has a very good prognosis for recovery (3-4months).

392
Q

What is axonotmesis?

A

Axon and myelin sheath disrupted but endoneurium and supporting structures intact → Wallerian degeneration of axon segment distal to injury. Axons can regenerate at 1-2mm/day. Better prognosis with distal injuries (less growth needed and nerve can survive).

393
Q

What is neurotmesis?

A

Nerve completely transected

394
Q

Conservative treatment of nerve entrapment?

A

Conservative: Prevent repeated stress/injury, physiotherapy, NSAIDs, local anesthesia/steroid injection

395
Q

Surgical treatment of nerve entrapment?

A

Surgical: Nerve decompression ± transposition for progressive deficits, muscle weakness/atrophy, failure of medical management

396
Q

Treatment of stretch/contusion peripheral nerve injuries?

A

Follow-up clinically for recovery; exploration if no recovery in 3 mo

397
Q

Treatment of axonotmesis peripheral nerve injuries?

A

If no evidence of recovery, resect damaged segment. Prompt physical therapy and rehabilitation to increase muscle function, maintain joint ROM, maximize return of useful function. Recovery usually incomplete

398
Q

Treatment of neurotmesis peripheral nerve injuries?

A
  • Surgical repair of nerve sheath unless known to be intact (suture nerve sheaths directly if ends approximate or nerve graft [usually sural nerve]).
  • Clean laceration: early exploration and repair.
  • Contamination or associated injuries: tag initially with nonabsorbable suture, reapproach within 10 d
399
Q

Etiology of movement disorders can be divided into:

A
  1. Hyperkinetic
  2. Bradykinetic
  3. Tremor
400
Q

Etiology of hyperkinetic movement disorders?

A
  • Tics
    • Primary (sporadic and inherited)
      • Tourette syndrome
      • Huntington disease
    • Secondary
      • Infections (e.g., encephalitis, Creutzfeldt-Jakob)
      • Drugs (e.g., stimulants, levodopa)
  • Dystonia
    • Primary (sporadic and inherited)
    • Dystonia plus syndromes (e.g., medication)
  • Stereotypies (typically with mental retardation or autism)
  • Chorea/Athetosis/Ballism
  • Essential tremor
  • Myoclonus
401
Q

Etiology of bradykinetic movement disorders?

A
  • Parkinson disease
  • Wilson disease
  • Huntington disease
402
Q

What is akathisia?

A

Subjective generalized restlessness relieved by voluntary stereotypic movements (e.g. squirming)

403
Q

What is chorea?

A

Brief, unpredictable, irregular movements, flowing from one body part to another; can appear purposeful in milder forms

404
Q

What is ballism?

A

Large-amplitude, involuntary, flinging movements that are most commonly unilateral (hemiballism) due to vascular lesion at STN

405
Q

What is athetosis?

A

Abnormal muscle contractions cause involuntary writhing movements, usually distally

406
Q

Description of the movement disorder

A
  • Rhythmicity
  • Speed
  • Duration (continuous vs episodic)
  • Location (distal or proximal)
  • Suppressibility
407
Q

What is the definition of a tremor?

A

Rhythmic oscillation of a body part around a joint with alternating contraction in agonist/antag muscle groups

408
Q

Clinical features of tremors?

A

Can be described as rhythmic, can be fast or slow, is continuous, distal (often involves the hand) and not suppressible

409
Q

How can tremors be classified?

A
  • Resting tremor
  • Action tremor
    • Postural tremor
    • Intention tremor
    • Task-specific tremor
    • Kinetic tremor
410
Q

Clinical features of resting tremor?

A
  • Characteristics: 3-7 Hz pillrolling
  • Worse with – rest while concentrating
  • Associated Sx: TRAP
411
Q

DDx of resting tremor?

A

PD, Parkinsonism, Wilson’s disease, mercury poisoning

412
Q

What is a postural tremor?

A

Occurs when a person maintains a position against gravity, such as holding the arms outstretched.

413
Q

Treatment of resting tremors?

A

Carbidopa-levodopa, surgery, DBS

414
Q

Clinical features of postural tremor?

A
  • Characteristics: 6-12 Hz fine tremor
  • Worse with – sustained posture (outstretched arms)
  • Associated Sx: Autosomal dominant FHx
415
Q

DDx of postural tremor?

A

Physiologic, essential, hyperthyroidism, hyperglycemia, heavy metal poisoning, CO poisoning, drug toxicity, sedative/alcohol withdrawal

416
Q

Treatment of postural tremor?

A

Propranolol, primidone, topiramate

417
Q

What is an intention tremor?

A

Produced with purposeful movement toward a target, such as lifting a finger to touch the nose. Typically the tremor will become worse as an individual gets closer to their target.

418
Q

Clinical features of intention tremor?

A
  • Characteristics: <5 Hz coarse tremor
  • Worse with – finger to nose
  • Associated Sx: Cerebellar findings
419
Q

DDx of intention tremor?

A

Cerebellar disorders, Wilson’s disease, MS, anticonvulsants, alcohol, sedatives

420
Q

What is a task-specific tremor?

A

Only appears when performing highly-skilled, goal-oriented tasks such as handwriting or speaking.

421
Q

What is a kinetic tremor?

A

Associated with any voluntary movement, such as moving the wrists up and down or closing and opening the eyes.

422
Q

Clinical features of an essential tremor

A
  • No additional symptoms predating tremor
  • Made better with alcohol
  • Present for years
  • Affects ability to do fine tasks, present all the time to some degree
  • Fast, small amplitude.
  • Present bilateral hands
  • Worse with posture, finger to nose, writing
423
Q

Clinical features of a cerebellar tremor

A

Cerebellar tremor is typically a slow, high-amplitude (easily visible) tremor of the extremities (e.g., arm, leg) that occurs at the end of a purposeful movement

424
Q

What is a psychogenic tremor?

A

Can appear as any form of tremor. The tremor increases in times of stress and decreases or disappears when distracted. Many individuals with psychogenic tremor have an underlying psychiatric disorder such as depression or post-traumatic stress disorder (PTSD).

425
Q

What is a physiologic tremor?

A

Physiologic tremor occurs in all healthy individuals. It is rarely visible to the eye and typically involves a fine shaking of both of the hands and also the fingers. It is not considered a disease but is a normal human phenomenon

426
Q

Etiology of Parkinson’s disease?

A
  • Sporadic: Combination of oxidative stress to dopaminergic neurons, environmental toxins (e.g. pesticides), accelerated aging, genetics
  • Familial (10%): autosomal dominant alpha-synuclein or LRRK2 mutations, autosomal recessive parkin, PINK1, or DJ-1mutation (juvenile onset)
  • MPTP(neurotoxin)
427
Q

Clinical features of Parkinsonian tremor?

A
  • Anosmia – loss of smell
  • REM Sleep Behaviour Disorder
  • New tremor
  • Noticed by others at first cause mostly present with rest
  • Doesn’t impair functioning as much (only present at rest)
  • Slow, present at rest
  • Unilateral
  • Disappears with movements
428
Q

Associated factors of Parkinson’s disease?

A
  • Risk: family history, male, head injury, rural living, exposure to certain neurotoxins
  • Protective: coffee drinking, smoking, NSAID use, estrogen replacement in post-menopausal women
429
Q

Pathophysiology of Parkinson’s disease?

A
  • Loss of dopaminergic neurons in pars compacta of substantia nigra – decreased dopamine in striatum - 1. disinhibition of the indirect pathway, and 2. decreased activation of the direct pathway - increased inhibition of cortical motor areas
  • alpha-synucleinopathy: alpha-synuclein accumulates in Lewy bodies and causes neurotoxicity in substantia nigra
430
Q

Key parkinsonism features

A

TRAP: Tremor (resting), Rigidity, Akinesia/bradykinesia, Postural instability

431
Q

Diagnostic criteria of Parkinson’s disease?

A
  • Bradykinesia with either rest tremor or rigidity
  • 2 or more supportive criteria (clear and dramatic beneficial response to dopaminergic therapy, levodopa- induced dyskinesia, rest tremor of a limb, olfactory loss/cardiac sympathetic denervation on MIBG scintigraphy)
  • Asymmetry of signs – starts unilateral, stays asymmetric although bilateral disease, absence of autonomic dysfunction/dementia/EOM abnormalities (early) with absence of other causes like drugs that block dopamine.
432
Q

Clinical features of Parkinson’s disease?

A
  1. Negative motor
    * Bradykinesia: slow, small amplitude movements, fatigue from rapid alternating movements, difficulty initiating movement, starts unilateral
  2. Positive motor
  • resting tremor: typically 4-6 Hz “pill-rolling” tremor, especially in hands
  • rigidity: lead-pipe rigidity with cogwheeling due to superimposed tremor
  1. Asymmetric onset of tremor, rigidity, bradykinesia
  2. Progressive course
  • related findings: masked facies, hypophonia, aprosody (monotonous speech), dysarthria, micrographia, shuffling gait with decreased arm swing
  • freezing of gait: occurs with walking triggered by initiating stride or barriers/destinations, lasting seconds
  • postural instability: late finding presenting as falls
  • cognition: bradyphrenia (slow to think/respond), dementia (late finding)
  • behavioural: decreased spontaneous speech, depression, sleep disturbances, anxiety
  • autonomic: constipation, urinary retention, sexual dysfunction, orthostatic hypotension, clinostatic hypertension
433
Q

What is the mainstay treatment of Parkinson’s disease?

A

REPLACE DOPAMINE: levodopa/carbidopa (Sinemet) or levodopa/benserazide (Prolopa)

434
Q

Adjuncts for Parkinson’s disease?

A

Dopamine agonists, MAOI, anticholinergics (especially if prominent tremors), catechol-O-methyltransferase inhibitors

435
Q

Surgical treatments for PD

A
  • thalamotomy
  • pallidotomy
  • deep brain stimulation (thalamic, pallidal, subthalamic) - this helps the motor symptoms
436
Q

Psychiatric treatment for PD?

A
  • SSRIs first line
  • TCAs (beware fall risk, cognitive impairment, and worsening symptoms of Parkinson’s disease)
437
Q

_____ is used as standard to treat the dyskinesia in Parkinson’s.

A

Amantadine

438
Q

Clinical features of progressive supranuclear palsy?

A

Tauopathy with limited vertical gaze (down gaze more specific) that can be overcome by the oculocephalic reflex, early falls, wide-based unsteady gait, axial rigidity; and akinesia, dysarthia, and dysphagia

439
Q

Clinical features of corticobasal syndrome?

A

Tauopathy with varied presentations but classically presenting with unilateral parkinsonism, dystonia/myoclonus, and apraxia ± “alien limbs” phenomenon; ¬± progressive non-fluent aphasia

440
Q

What are the two subtypes of multiple system atrophy and their features?

A

Synucleinopathy presenting as either cerebellar predominant (MSA-C, previously olivopontocerebellar atrophy) or parkinsonism predominant (MSA-P, previously nigrostriatal degeneration); both are associated with early autonomic dysfunction (blood pressure, breathing, bladder function and muscle control)

441
Q

Clinical presentation of vascular parkinsonism?

A

Multi-infarct presentation with gait instability and lower body parkinsonism; less likely associated with tremor

442
Q

What is seen on MRI for multiple system atrophy?

A

Atrophy of putamen/cerebellum and putaminal hypointensity with rim hyperintensity on T2W – with HOT CROSS BUN SIGN in basis pontis

443
Q

What is myoclonus?

A

Sudden, brief, shock-like movement that is nonsuppressible. Faster than tic, usually distal limbs.

444
Q

What are the types of myoclonus?

A
  • Focal – single body part
  • Segmental – 2+ contiguous body regions (body parts close together)
  • Multifocal – 2+ regions, not contiguous
  • Generalized - we can kind of experience this when falling asleep and having a jerk that wakes you up
445
Q

What is nocturnal myoclonus?

A

Characterized by recurrent episodes of frequent limb movements while sleeping. It mostly happens in the lower parts of the body like the toes, ankles, knees and hips.

446
Q

DDx of myoclonus?

A

Commoner causes of myoclonus that may be seen in primary care include: medication side effects, toxin or chemical ingestion, metabolic encephalopathy, hypoxic-ischemic encephalopathy, myoclonus in the elderly, in the setting of an epilepsy syndrome

447
Q

What is dystonia?

A

Co-contraction of agonist and antagonist muscles causing sustained twisting movements which can be tonic (dystonic postures) or phasic (dystonic movements)

448
Q

Etiology of primary dystonia?

A

familial, sporadic (torticollis, blepharospasm, writer’scramp)

449
Q

Etiology of dystonia-plus syndromes?

A

Dystonia-plus syndromes results from nondegenerative, neurochemical disorders associated with other neurological conditions; dopa-responsive dystonia, myoclonus-dystonia

450
Q

Etiology of secondary dystonia?

A

Thalamotomy, stroke, CNS tumour, demyelination, PNS injury, drugs/toxins (L-dopa, neuroleptics, anticonvulsants, Mn, CO, cyanide, methanol)

451
Q

Etiology of heredodegenerative dystonia

A

Heredodegenerative dystonia generally results from neurodegenerative disorders in which other neurological symptoms are present and in which heredity plays a role. Parkinsonian disorders, Wilson’s disease, Huntington

452
Q

Clinical features of dystonia?

A
  • Sustained or intermittent twitching movements caused by co-contraction of agonist and antagonist muscles
  • Symptoms exacerbated by fatigue, stress, and emotions; relieved by sleep or specific tactile/ proprioceptive stimuli (‘geste antagoniste’, e.g. place hand on face for cervical dystonia)
  • More likely to be progressive and generalized if younger onset or leg dystonia
453
Q

Local medical treatment of dystonia?

A

Local medical: botulinum toxin

454
Q

Systemic medical treatment of dystonia?

A

Systemic medical: anticholinergics (benztropine), muscle relaxants (baclofen), or benzodiazepines, dopamine depletors (tetrabenazine); dopamine for dopa-responsive dystonia

455
Q

Surgical treatment of dystonia?

A

Surgical: surgical denervation of affected muscle, stereotactic thalamotomy (unilateral dystonia), posteroventral pallidotomy, or DBS

456
Q

Etiology of Huntington’s disease?

A

Genetics: autosomal dominant CAG repeats (with anticipation) in huntingtin (HTT) gene on chromosome 4, which leads to accumulation of defective protein in neurons

457
Q

Pathogenesis of Huntington’s disease?

A

Global cerebral atrophy, especially affecting the striatum, leading to increased activity of the direct pathway, and decreased activity of the indirect pathway

458
Q

Clinical features of Huntington’s disease?

A
  • Typical progression: insidious onset with clumsiness, fidgetiness, and irritability, progressing over 15yr to major NCD, psychosis, and chorea
    • major NCD: progressive memory impairment and loss of intellectual capacity
    • chorea: begins as movement of eyebrows and forehead, shrugging of shoulders, and parakinesia (pseudo-purposeful movement to mask involuntary limb jerking)
    • Progresses to dance-like or ballism, and in late stage is replaced by dystonia and rigidity
    • Mood changes: irritability, depression, anhedonia, impulsivity, bouts of violence
459
Q

Juvenile-onset HD (Westphal variant) characterized by

A

Parkinsonism, dystonia, rigidity, seizures

460
Q

Investigations for Huntington’s disease?

A
  • MRI
    • enlarged ventricles, atrophy of cerebral cortex, and caudate nucleus
  • Genetic testing
    • expansion of the cytosine-adenine-guanine (CAG) trinucleotide repeats in the HTT gene
    • CAG repeats (>28) on chromosome 4p16.3 that encodes the protein huntingtin
461
Q

Treatment of Huntington’s disease?

A
  • No disease-altering treatment
  • Psychiatric symptoms: antidepressants and antipsychotics
  • Chorea: neuroleptics and benzodiazepines
  • Dystonia: botulinum toxin
462
Q

Clinical features of tic?

A

Suppressible, distractible, suggestible, variable, worsen with stress or excitement, premonitory urge - describe something that predicts something bad will happen

463
Q

What is the definition of tics?

A

A tic is a sudden, rapid, recurrent, nonrhythmic, stereotyped motor movement or vocalization

464
Q

Common criteria of tic disorders?

A
  • tics may wax and wane in frequency but have persisted for an extended period of time
  • onset is <18 yr
  • disturbance is not attributable to the physiological effects of a substance or another medical condition
465
Q

Diagnostic criteria of Tourette’s syndrome?

A

Multiple motor and >1 vocal tics that have persisted for >1yr since onset

466
Q

Etiology of Tourette’s syndrome?

A
  • Genetic factors: >55% concordance rate in monozygotic twins.
  • Prenatal/perinatal factors: Older paternal age, obstetrical complications, maternal smoking, and low birth weight.
  • Psychological factors: Symptom exacerbations with stressful life events.
467
Q

Treatment of Tourette’s disorder?

A
  • Psychoeducation.
  • Behavioral interventions-habit reversal therapy.
  • Medications-utilize only if tics become severely impairing or also treating comorbidities. Due to the fluctuating course of the disorder, it can be difficult to determine medication efficacy.
  • Alpha-2 agonists: guanfacine (first choice), clonidine (more sedating).
468
Q

Diagnostic criteria of persistent (chronic) motor or vocal tic disorder?

A

Single or multiple motor or vocal tics (but not both motor and vocal) that have persisted for >1 yr since onset

469
Q

Diagnostic criteria of provisional tic disorder?

A

Single or multiple motor and/or vocal tics present for <1yr since first tic onset

470
Q

DDx for secondary tic disorders

A

Encephalitis, CJD, Sydenham’s chorea, head trauma, drugs, mental retardation syndromes

471
Q

What are simple and complex tics?

A
  • Simple tics: short duration (msec)
  • Complex tics: longer (seconds), more purposeful and often include a combination of simple tics
472
Q

Types of motor tics?

A
  • simple: blinking, head jerking, shoulder shrugging, extension of the extremities
  • dystonic: bruxism (grinding teeth), abdominal tension, sustained mouth opening
  • complex: copropraxia (obscene gestures), echopraxia (imitate gestures), throwing, touching
473
Q

Types of vocal tics?

A
  • simple: blowing, coughing, grunting, throat clearing
  • complex: coprolalia (shout obscenities), echolalia (repeat others’ phrases), palilalia (repeat own phrases)
474
Q

Treatment of tic disorders?

A

Dopamine blockers, dopamine depletors (tetrabenazine), clonidine, clonazepam, or DBS

475
Q

Define language disorders?

A

Patients with impairment in comprehension and/or use of the form, content, or function of language

476
Q

Define speech disorders?

A

Patients with impaired articulation, fluency and voice

477
Q

DDx for language disorders?

A
  • Delayed and developmental language impairment (e.g., deafness, autism spectrum disorder, neglect, abuse)
  • Degenerative, vascular, or other central nervous system disorders (e.g., stroke)
  • Head injury
478
Q

DDx for speech disorders?

A
  • Articulation disorder (e.g., dysarthria)
  • Fluency (e.g, stuttering, Parkinson disease)
  • Speech apparatus lesions (e.g., cleft palate, head and neck neoplasm)
479
Q

Define aphasia

A

An acquired disturbance of language characterized by errors in language production, writing, comprehension, or reading

480
Q

Broca’s area (posterior inferior frontal lobe) is involved in?

A

Language production (expressive)

481
Q

Wernicke’s area (posterior superior temporal lobe) is involved in?

A

Comprehension of language (receptive)

LMCC (23 decks)

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