Neurology Flashcards
What is the pharmacological management of delirium?
- 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)
What could be used as a reversal agent for benzodiazepines?
Flumazenil
Which way do the eyes nystagmus with cold/hot water for vestibulo-ocular reflex
- 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
For the oculocephalic reflex; turning head should elicit conjugate movement of gaze away from direction of turn. If not then what do you suspect?
brainstem function not intact
What are the cadiac investigations if you suspect ACS?
ECG, CK, troponin
List the GSC eye responses
Spontaneously (+4) To verbal command (+3) To pain (+2) No eye opening (+1)
What is the 4AT exam for delirium?
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
Initial management of coma?
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
What are some risk factors for delirium?
Dementia/brain disease, polypharmacy, elderly, organ failure, hospitalization
Ddx for delirium
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
What are the criterias of Confusion Assessment Method (CAM)?
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
About half the cases of NMDA receptor encephalitis are due to?
About half of cases are associated with tumors, most commonly teratomas of the ovaries.
List the GSC motor responses
Obeys commands (+6) Localizes pain (+5) Withdrawal from pain (+4) Flexion to pain (+3) Extension to pain (+2) No motor response (+1)
Chronic management considerations for coma
▪ 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.
Three subtypes of delirium?
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
What is Lewy-Body Dementia?
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).
What breathing pattern might you see you a diencephalon injury?
Cheyne-Stokes
List the GSC verbal responses
Oriented (+5) Confused (+4) Inappropriate words (+3) Incomprehensible sounds (+2) No verbal response (+1)
Sx of normal pressure hydrocephalus
Wet, wacky, and wobbly - Triad of dementia, gait disturbance and urinary incontinence
How to perform Hoffman’s Reflex
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
What could be used as a reversal agent for opioids?
Naloxone
What are the symptoms of NMDA receptor encephalitis?
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.
What is unique about the gait in normal pressure hydrocephalus
Gait is unique – cant lift legs off ground, but if lying down can mimic walking
What are the investigations (basic) you would do for delirium?
LABS CBCD, lytes, urea, Cr, glucose, Ca, urinalysis IMAGING CXR, head CT MICROBIOLOGY urine C&S, blood C&S (if any fever)
Mnenomic for GCS
My Extra Value Meal costs $4.56
What is NMDA receptor encephalitis?
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.
What is Non-Convulsive Status Epilepticus?
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.
Investigations for coma?
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
What would you suspect for cerebral and brainstem damage with the vestibulo-ocular reflex?
▪ Cerebral Damage: fast phase absent, deviation to same side if cold water ▪ Brainstem Damage: fast + slow phase absent
Tx of normal pressure hydrocephalus
Treat with CSF drain (30-40 cc’s) and place a VP shunt
Definition of coma
Coma refers to a state of unresponsiveness without arousal caused by interruption of neuronal networks that regulate consciousness.
What are the investigations if you suspect liver disease?
AST, ALT, ALP, bilirubin, INR, PTT, NH4
Physical exam of coma?
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
What are the neurological mimics of delirium?
Non-Convulsive Status Epilepticus Aphasia Lewy-Body Dementia Encephalitis
What is the environmental management of delirium?
- 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
Ddx of coma
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
Pathophysiology of hearing loss?
- 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
Most common causes of hearing loss?
Cerumen accumulation, Noise, Aging (Presbycusis), Infections (particularly among children and young adults)
Congenital causes of hearing loss?
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
Acquired causes of hearing loss?
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)
What is otosclerosis and age of onset
Abnormal bone growth inside the ear, FHx, age of onset 20-30s
Waardenburg syndrome signs
White forelock of hair or different colored eyes
Pendred syndrome signs
Associated with thyroid gland disorders, SLC26A4 gene, enlarged vestibular aqueducts
High Risk Factors for hearing loss in newborns
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
Who should be screened for hearing loss
All infants
Important history points for hearing loss
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).
What should be included for the physical exam of hearing loss?
External ear + TM inspection, Neuro exam (particular attention needs to be paid to the 2nd through 7th cranial nerves). Weber + Rhine testing
Which cranial nerves are also affected by tumors that involve the 8th nerve
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
How is the weber test performed?
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)
Weber Test lateralization
Weber Test lateralization = ipsilateral conductive hearing loss or contralateral sensorineural loss
Weber = lateralizes to left Rinne = AC>BC (+) bilaterally
Right-sided SNHL, normal left ear
Weber = central Rinne = AC>BC (+) bilaterally
Normal or bilateral SNHL
What is the Rinne test. What’s normal?
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)
Puretone pattern for conductive hearing loss?
- BC in normal range - AC outside of normal range - Gap between AC and BC thresholds >10dB (an air-bone gap)
Puretone pattern for sensorineural hearing loss?
- Both air and bone conduction thresholds below normal - Gap between AC and BC <10 dB (no air-bone gap)
Puretone pattern for mixed hearing loss?
- Both air and bone conduction thresholds below normal - Gap between AC and BC threshold s>10dB (an air-bone gap)
What is presbycusis?
SNHL associated with aging (starting in 5th and 6th decades)
Clinical features of presbycusis?
- 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
Tx of hearing loss
- 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
Prevention of hearing loss
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).
Delirium vs dementia
What is a primary headache?
No identifiable cause
What is a secondary headache?
Underlying etiology present
What should be included on hx for a patient with a headache?
- 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)
Physical exam for a patient presenting with headache?
- Vitals: is there fever? Is there severe HTN (sBP >180 or dBP >120)?
- Fundoscopy
- Focal Neuro Exam
- Is there papilledema? Consider carotid artery dissection
What are the red flags for headache?
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
When is neuroimaging (CT) required for headaches?
If red flags or risk of herniation (i.e. intracranial pathology)
When would you use MRI w/ or w/o contrast for headache?
If immunocompromised, if >60 with suspect temporal arteritis
When would you do a lumbar puncture with a patient presenting with headache?
- If suspect infection (WBCs), bleeding (RBCs), or malignancy (abnormal cells)
Predictors of migraine Dx
POUND: Pulsating/throbbing, 4-72 hOurs, Unilateral, Nausea/vomit, Disabling
Criteria for migraine headache
2/3: nausea/vomiting, photophobia, or worse w/ exercise
How might a migraine headache present in children?
Cyclical vomiting, episodic stomach pain.
Two types of migraine headaches?
- Aura
- Without aura
Symptoms of aura headache?
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
What is cortical spreading depression?
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
What are some lifestyle changes for the treatment of headaches?
Lifestyle (caffeine – drink same amount everyday, sleep – change in hours of sleep triggers, diet, triggers, exercise), headache diary + stress management
What is the hierarchy for abortive treatment for headache?
Hierarchy: Ibuprofen, naproxen, Tylenol → triptans → naproxen sodium + triptan, narcotic analgesic are not recommended.
When should a patient use abortive therapy?
Use at headache onset and hit it hard, not daily otherwise you can make their migraine transform to daily.
When is prophylactic medication indicated for migraines?
Indicated if headache >3 days/month and acute meds not effective OR >8 days/month OR Disability despite acute meds
What are 1st line prophylactic treatments for headaches?
1st line: propanolol, metoprolol (avoid in asthma), amitryptiline (consider if depression, anxiety, insomnia)
What are 2nd line prophylactic treatments for headaches?
2nd line: topiramate (1st line if overweight), candesartan (avoid in pregnancy)
What are other prophylactic treatments for headaches?
Other: divalproex sodium (avoid in pregnancy), pizotifen (monitor for somnolence and weight gain), botox (chronic headache only)
Symptoms of tension headaches?
Squeezing sensation (tight-band), bilateral, fronto-occipital or generalized, no N/V, no photophobia, no migrainous Sx, not worse with activity
What is defined as chronic tension headaches?
>15 days/month for >6 months
What are the abortive and prophylactic treatments of tension headaches?
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))
What are the symptoms of cluster headaches?
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
What are the abortive and prophylactic treatments of cluster headaches?
Abortive: triptans, oxygen 100%
Preventative: verapamil 120-900mg – get ECG, lithium carbonate, valproate, topiramate, melatonin
What is transitional treatment for cluster headaches and when is it used?
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)
What is the presentation of increased ICP?
Consistent headache worse in AM, whooshing in ears, papilledema + focal neuro deficits
Who does increased ICP usually affect?
Typically in young overweight women
What do you need to rule out with increased ICP sx and with what test?
CT venogram (rule out venous sinus thrombosis)
Treatment for increased ICP
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.
Sx of thunderclap headache?
Acute onset, reaches max intensity within minutes, worse with exertion
Causes of thunderclap headache
Causes: SAH and arterial dissection
Sx of meningitis and/or encephalitis?
Fever/chills, nuchal rigidity, photophobia, N/V, confusion/altered LOC, rash, immunocompromised
Sx of temporal arteritis
50yo localized headache (temporal), jaw claud, scalp tenderness tender temporal artery, PMR association, visual symptoms.
Investigations for temporal arteritis?
Temporal artery biopsy and CRP.
Tx for temporal arteritis?
Immediate high-dose moderate corticosteroids (prednisone)! Can lead to permanent blindness.
What is considered medication overuse for headaches?
- Ergots, triptans, combination analgesics or codeine/other opioids ≥ 10 days a month OR
- Acetaminophen or NSAIDs ≥ 15 days a month
What are the indications for urgent LP?
- Suspected CNS infection (with the exception of brain abscess or a parameningeal process).
- Suspected SAH in a patient with a negative CT scan
What are some contraindications for LP?
- Possible raised intracranial pressure (ICP) with risk for cerebral herniation
- Thrombocytopenia or other bleeding diathesis, including ongoing anticoagulant therapy
- Suspected spinal epidural abscess
Definition of stroke?
Sudden onset of neurological deficits of a vascular etiology with infarction of CNS tissue
Definition of TIA?
- 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)
Two types of stroke?
- Ischemic (85%)
- Hemorrhagic (15%)
Etiology/causes of ischemic stroke?
- 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)
Etiology/causes of hemorrhagic stroke?
- 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
ACA stroke syndrome?
Contralateral leg paresis, sensory loss, cognitive deficits (e.g. apathy, confusion, and poor judgment). Right hemi – neglect. Left hemi – aphasia. Sensory loss + incontinence
Systemic hypoperfusion primarily affects which areas?
Primarily affects watershed areas (between the major cerebral arterial territories)
Mechanism by which small vessel/lacunar causes a stroke?
Chronic HTN and DM cause vessel wall thickening and decreased luminal diameter
MCA stroke syndrome?
- contralateral weakness and sensory loss of face and arm
- cortical sensory loss
- may have contralateral homonymous hemianopia or quadrantanopia
- if dominant (usually left) hemisphere: aphasia
- if non-dominant (usually right) hemisphere: neglect
- eye deviation towards the side of the lesion (away from the weak side)
PCA stroke syndrome?
- contralateral hemianopia or quadrantanopia
- midbrain findings: CN III and IV palsy/pupillary changes, hemiparesis
- thalamic findings: sensory loss, amnesia, decreased LOC
- if bilateral: cortical blindness or prosopagnosia
- hemiballismus
Proximal basilar artery stroke syndrome?
Proximal (usually thrombosis): impaired EOM, vertical nystagmus, reactive miosis, hemi- or quadriplegia, dysarthria, locked-in syndrome, coma
Distal basilar artery stroke syndrome?
Distal (usually embolic, i.e. top of the basilar syndrome): somnolence, memory and behaviour abnormalities, oculomotor deficit
PICA (lateral medullary or Wallenberg syndrome) stroke syndrome?
Ipsilateral ataxia, ipsilateral Horner’s, ipsilateral facial sensory loss, contralateral limb impairment of pain and temperature sensation, nystagmus, vertigo, nausea/vomiting, dysphagia, dysarthria, hiccups
Medial medullary infarct stroke syndrome?
Contralateral hemiparesis (facial sparing), contralateral impaired proprioception and vibration sensation, ipsilateral tongue weakness
Subcortical/lacunar infarcts stroke syndrome?
Contralateral weakness without cortical deficits since the stroke is now subcortical. Face/arm/leg equally involved.
Small vessel occlusions are lacunar strokes (20%) due to ______ (vessels thicken usually from HTN, DM2).
Lipohyalinosis
General assessment/physical exam for stroke/TIA?
- 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
Mimics to rule out for stroke/TIA?
Seizure/post-ictal, hypoglycemia, migraine, conversion disorder
Investigations for stroke/TIA?
- 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)
CT imaging findings of ischemic stroke?
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
Hemorrhagic stroke CT imaging findings
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!
Acute stroke management includes?
- Thrombolysis
- Anti-Platelet Therapy
- Acute Anti-Coagulant Therapy
- Intra-Arterial Mechanical Thrombectomy
rtPA (recombinant tissue plasminogen activator) should be given within ___ of acute ischemic stroke onset provided there are clinical indications and no contraindications to use
4.5 h
Contraindications to rtPA (recombinant tissue plasminogen activator)?
- 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
Who should receive ASA for stroke and what is the loading dose?
- 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)
For patients with TIA or stroke and atrial fibrillation, if rtPA not received:
- 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
Eligibility for early thrombectomy
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!!
Other acute management issues for stroke?
- 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
Blood pressure control for stroke?
- 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
Top 6 symptoms likely to be TIA?
*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)
- Monocular or Hemifield Visual Loss: not blurring of entire visual field
- Double Vision, Crossed Numbness or Weakness, Slurred Speech, Ataxia of Gait. Localizes to the brainstem.
- Hemibody Numbness
- Vertigo: only if present with brainstem sx
Symptom unlikely to be TIA?
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.
Features supportive of TIA/Stroke?
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
What is the ABCD2 Risk Score?
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
Highest risk TIA is defined as?
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)
High risk TIA is defined as?
TIA symptoms in the last 48 hours to 2 weeks with high risk sx (speech disturbance or weakness of the face, arm or leg)
Moderate risk TIA is defined as?
TIA symptoms in the last 48 hours to 2 weeks with lower risk symptoms (hemianopsia, monocular visual loss, brainstem syndrome)
Lower risk TIA is defined as?
TIA symptoms more than 2 weeks ago regardless of symptoms
Immediate actions for highest risk TIA?
Emergent assessment (brain and vascular imaging – CTA neck vessels or carotid doppler) should be done within hours. Immediate EKG and antiplatelet therapy.
Immediate actions for high risk TIA?
24 hours to get a clinical assessment done and then vascular imaging and brain imaging. EKG and immediate antiplatelet therapy.
Immediate actions of moderate risk TIA?
Investigation by a stroke expert within two weeks of first contact. Brain imaging and vascular imaging within 2 weeks. EKG and immediate antiplatelet therapy.
Immediate actions of lower risk TIA?
Referral to clinic with neurological expertise to be seen within 1 month
Post-TIA treatment?
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
Secondary prevention of ischemic stroke anti-platelet therapy?
- Initial choice: ASA
- If cerebrovascular symptoms while on ASA or if unable to tolerate ASA: Aggrenox, clopidogrel
Secondary prevention of ischemic stroke carotid stenosis?
- 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.
Secondary and primary prevention of ischemic stroke atrial fibrillation?
- 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
Secondary and primary prevention of ischemic stroke HTN?
- 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
Secondary and primary prevention of ischemic stroke hypercholesterolemia?
- 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
Secondary and primary prevention of ischemic stroke smoking?
- 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
Etiology of gait disturbances?
- Cerebellar ataxia
- Tumors
- Vascular
- Hereditary
- Multiple sclerosis
- Drugs
- Alcohol
- Sensory ataxia
- Vestibular
- Proprioceptive
- Visual
- Other disorders of locomotion
- Other central nervous system (e.g., cerebral)
- Parkinson’s disease
Physical exam for gait disturbance?
- 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)
Red flags of gait disturbance?
Sudden onset, cerebellar ataxia, paresis (hemi-, para- or quadri-), bowel/bladder incontinence
What is an antalgic gait?
Painful limb, decreased stance phase; quick/short steps
What is a high steppage/foot drop gait?
Distal weakness esp. dorsiflexors, difficulty clearing toes in swing phase→ audible double slap
What is a spastic hemiplegic gait?
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
What is a Trendenburg gait?
Proximal muscle weakness of hip abductors, pelvis excessively drops on unaffected limb during swing, to clear toes→ excessively laterally bend trunk on affected side
What is a waddling gait?
When the trendelenburg gait is bilateral in conditions such as Muscular dystrophies or Myopathies then they demonstrate bilateral excessive lateral trunk bending
What is an ataxic gait?
Unsteady on feet→ is wide based (patients overshoot or undershoot with each step.)
What is an parkinsonian gait?
Slow start, trunk bent forward, legs and arms stiff with short shuffling steps (aka festinating)
What is a scissoring gait?
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.
Clinical features of myopathy?
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
Etiology of myopathies related to gait disturbance?
Muscular dystrophy, autoimmune disorders, myasthenia gravis (neuromuscular junction)
Clinical features of neuropathy?
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
Etiology of neuropathies related to gait disturbance?
Diabetic neuropathy, hereditary neuropathies (Charcot-Marie-Tooth Disease), Guillian Barre syndrome, peroneal n. injury, L5 radiculopathies
Etiology of Parkinsonism gait?
PD, neuroleptic-induced
Which etiologies cause chorea?
Huntington’s disease
What is chorea?
Variable steps, poor balance. movement disorder that causes involuntary, unpredictable body movements.
What is dystonia?
Involuntary posturing of the feet brought on by actions or intentions.
Which etiologies cause dystonia?
Cerebral palsy, birth injury, prenatal injury.
What is a diplegic gait?
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.
Which etiologies cause diplegic gait?
Cerebral palsy
Etiologies that cause hemiplegic gait?
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.
What is cerebellar ataxia?
Patients can show dysmetria and intention tremor (only present during movement) on upper and lower limb testing (finger nose/heel shin). Ataxic gait
Etiologies that cause cerebellar ataxia?
Alcoholic cerebellar degeneration (midline), stroke, tumor, demyelination
What is defined as a cautious gait?
Most common ‘gait disorder’, adaptation to impairment, slower, short stride length, wide base – like walking on ice. Non-specific. May be associated with aging.
Clinical features of congenital cerebellar ataxias?
Early onset non-progressive ataxias associated with various syndromes as well as developmental abnormalities (e.g. Arnold-Chiari malformation, Dandy-Walker cysts)
Etiologies of acquired cerebellar ataxias?
- 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)
Etiologies of hereditary autosomal recessive ataxia?
Friedrich’s ataxia, ataxia with oculomotor apraxia, ataxia telangiectasia, vitamin E deficiency
Signs of Friedrich’s ataxia?
Signs: gait and limb ataxia, weakness, areflexia, extensor plantar reflex, impaired proprioception and vibration, dysarthria
Most common hereditary autosomal dominant ataxia?
Most commonly spinocerebellar ataxias (SCAs); 30+ types, most commonly due to CAG repeats
Signs of hereditary autosomal dominant ataxia?
Ataxia and dysarthria, chorea, polyneuropathy, pyramidal and/or extrapyramidal features, dementia
Definition of syncope?
Syncope is a sudden transient self-limited loss of consciousness from global cerebral hypoperfusion with spontaneous recovery
Clinical features that differ seizure from syncope?
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)
Clinical features that differ stroke from syncope?
Weakness, numbness, visual changes, CN symptoms (diplopia, dysphasia, dysarthria) other focal neuro deficits, CVA risk factors (HTN, CAD, DM, DLD, Afib, obesity)
Clinical features that differ SAH from syncope?
Sudden onset, severe headache (thunderclap), nausea/vomiting, photophobia, CN palsy (III, IV)
DDx for syncope?
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
Clinical features indicating a valvular etiology of syncope?
Sudden-onset syncope during exertion (HOCM) or when supine – may have CP, dyspnea, palpitations. FHx of sudden death, PMHx - HTN
Clinical features indicating a arrhythmic etiology of syncope?
Usually sudden and unprovoked (may have preceding palpitations). FHx of sudden death, PMHx - cardiac risk factors
Triggers of carotid sinus hypersensitivity
Triggers: head rotation/pressure on carotid sinus (shaving, tight collar)
Triggers of situational syncope?
Triggers: walking, defecation, micturition, prolong standing, after exercise, history similar events
Triggers of vasovagal syncope?
Triggers: Fear, heat, pain, stress, coughing, sneezing, GI stimulation/micturition (straining on BM or urine)
Investigations for syncope?
- 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