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65 Cards in this Set
- Front
- Back
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What are the most common brain tumors in adults? children?
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Adults: glioblastoma multiforme, astrocytoma, meningioma
Children: astrocytoma, medulloblastoma, ependymoma |
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What structures compose the diencephalon?
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Thalamus
Hypothalamus Subthalamus |
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How much volume of CSF is produced per day? How much is circulating at any given time?
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500 ml produced/day
150 ml circulating at a time |
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What structures is the telencephalon composed of?
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Cerebrum
Basal ganglia |
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What is the name of the passage that connects the lateral ventricles to the third ventricle?
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Foramen of Monro
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Which one causes more atrophy: UMN or LMN lesions?
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LMN causes severe atrophy.
UMN causes mild atrophy. |
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Which part of the nervous system is able to regenerate - CNS or PNS?
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Peripheral nervous system.
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Classification of sensory nerve fibres.
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General vs alternate classification:
Aα = Ia Aα = Ib Aβ = II Aγ = II Aδ = III C = IV |
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Latin names for forebrain, midbrain and hindbrain.
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Forebrain = prosencephalon
Midbrain = mesencephalon Hindbrain = rhombencephalon |
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What are the subtypes of Guillain Barre Syndrome?
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AIDP (acute inflammatory demyelinating polyneuropathy)
Miller Fisher syndrome AMAN (acute motor axonal neuropathy) AMSAN (acute motor and sensory axonal neuropathy) |
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What is typically found in Guillain Barre on LP CSF analysis?
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High protein.
Normal WBC. Normal RBC. Normal glucose. |
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Clinical features of Miller Fisher Syndrome.
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MFS is a variant of Guillain Barre Syndrome.
Ophthalmoplegia, ataxia, areflexia. |
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What are the disease modifying therapies for Guillain Barre Syndrome?
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Plasma exchange or IVIG.
Should choose one or the other. |
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How many spinal nerve pairs are there?
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31 total
8 cervical 12 thoracic 5 lumbar 5 sacral 1 coccygeal |
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What spinal level of fibres travel in the fasciculus cuneatus vs gracilis?
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cuneatus = above T6
gracilis = T7 and below |
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What is Clarke's nucleus?
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Also called dorsal nucleus.
It is where spinocerebellar fibres arise from. Extends from C8-L3. Located in the lateral horn. |
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Which arteries arise from the vertebral arteries?
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Anterior spinal artery, 2 posterior spinal arteries, PICA
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Which arteries arise from the basilar artery?
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AICA, pontine arteries, superior cerebellar arteries.
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At what level does the fasciculus cuneatus appear?
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T6
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At what level of the spinal cord does the dorsal column fibres synapse with nucleus gracilis/cuneatus, and cross as internal arcuate fibres?
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Caudal medulla
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Which muscles are affected first in upper/lower limbs in an UMN lesion?
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Extensors in upper limbs, flexors in lower limbs.
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What parts form the hippocampal formation?
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Dentate gyrus
Hippocampus Subiculum |
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Types of disease pattern in MS.
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Relapsing remitting
Secondary progressive Primary progressive Progressive relapsing |
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How do MS plaques appear on T1 weighted MRI? T2?
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T1 - hypointense.
T2 - hyperintense. |
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What are normal CSF values?
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WBCs 0-5 / mm3, 70% lymphocytes, 30% monocytes
Protein 140-520 mg/L IgG 10-80 mg/L Glucose 2.2-4.5 mmol/L |
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Treatment of MS
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Acute: steroids
Disease modifying therapy: -Interferon (Betaseron) -Glatiramer acetate (Copaxone) -Natalizumab (but can cause PML) |
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Syndrome of nondominant inferior parietal lobule.
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1. Topographic memory loss
2. Anosognosia 3. Construction apraxia 4. Dressing apraxia 5. Contralateral sensory neglect 6. Left hemianopia |
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What is normal ICP?
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10-15 mmHg
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What is it called when there is a layer of red-yellow after CSF is centrifuged?
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Xanthochromia.
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Immediate lab studies for any patient with suspected stroke.
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1 Noncontrast CT
2 ECG 3 CBC 4 Troponin 5 Electrolytes, urea nitrogen, creatinine 6 Serum glucose 7 PTT, INR 8 Partial thromboplastin time 9 Lipid profile |
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What drugs/antibiotics to give empirically for suspected bacterial meningitis?
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Dexamethasone 0.15 mg/kg IV stat.
Ceftriaxone 2 mg IV q12h. Vancomycin 2 mg IV q12h. Ampicillin 2 mg IV q4h. |
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What tests to order stat for patient arriving in active seizure.
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1. CBC, lytes
2. Mg, Ca 3. Glucose 4. AED levels 5. Toxicology screen 6. Alcohol |
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What is initial drug therapy for patient arriving in active seizure?
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Lorazepam 4 mg IV at rate of 2mg/min. Repeat dose in 5-10 mins if seizures continue. Max 8 mg.
-child 0.05-0.10 mg/kg, max 4 mg. May give IM midazolam or PR diazepam 5-10 mg if IV cannot be established. |
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What drug to give if seizure persists 16-35 mins?
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Fosphenytoin (Cerebyx) 20 mg PE/kg IV, at rate of 150 mg PE/min.
Can also be given IM at same dose. |
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What to do if seizure persists >= 36 minutes despite drug therapy?
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Intubate, consult anesthesia.
EEG monitoring. Rapidly administer pentobarbital, midazolam, or propofol in ICU. If no other option, then give phenobarbital 5 mg/kg/dose q15-30 mins, max 30 mg/kg. |
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Contraindications for LP.
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Cardiorespiratory compromise.
Cerebral herniation, increased ICP. Coagulopathy. |
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What needle gauge and length are used in adults for LP?
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22 gauge, 3.5 inch.
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Which glycogen storage disorders are associated with clinically significant muscle disease?
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Pompe's disease
Cori's disease McArdle's disease Tarui's disease |
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What is Shy-Drager syndrome?
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Orthostatic hypotension, anhidrosis, impotence, bladder atonicity.
Caused by degeneration of preganglionic sympathetic neurons from the intermediolateral cell column. |
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What is Cushing's response?
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Response to increased ICP.
Hypertension, bradycardia, irregular breathing. |
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Dosing and side effects of phenytoin.
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300 mg po qhs.
1. Gingival hypertrophy 2. Hursuitism 3. Rash 4. LFT abnormality 5. Adenopathy 6. Nystagmus 7. Ataxia |
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MOA of gabapentin.
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Binds to α₂δ-1 subunits of presynaptic voltage-gated Ca2+ channels.
Reduces release of glutamate, NE, substance P, and CGRP |
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Dosing and side effects of valproic acid as an antiepileptic drug.
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250-2000 mg PO qid.
1. Nausea 2. Weight gain 3. Hair loss 4. Tremor 5. Hepatitis 6. Agranulocytosis 7. Thrombocytopenia 8. SJS |
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Percentage of brain tumors that are primary vs metastatic.
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66% primary
33% metastatic |
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Significance of MGMT in glioblastoma multiforme.
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Determination of MGMT status may be predictive for response to alklylating agents.
Low MGMT levels/activity means favourable response to temozolomide. |
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What is Wada test?
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Done for patients who are being considered for surgical treatment for temporal lobe epilepsy.
Amytal (amobarbital) is injected into one common carotid artery. This inhibits the injected hemisphere for ~10 minutes. Language is tested, presence or absence of aphasia is noted. This determines which is the dominant hemisphere. Apparently no longer used. Instead, they use neuropsychiatric testing or PET scanning. |
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Idiopathic inflammatory myopathies
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Inclusion body myositis
Dermatomyositis Polymyositis |
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Potential clinical presentations of neurosarcoidosis.
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1. Cranial mononeuropathy.
2. Hypothalamic inflammation - polyuria, thirst, abnormal temperature, sleep, appetite. 3. Seizures. 4. Cognitive and behavioural change. 5. Meningitis. 6. Myelopathy or radiculopathy. 7. Carpal tunnel syndrome. |
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Most common causes of peripheral vertigo.
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1. BPPV
2. Migrainous vertigo 3. Vestibular neuritis 4. Meniere's disease |
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What are 3 clinical tests that are useful for determining peripheral vs central vestibular dysfunction?
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Head thrust
-supports unilateral peripheral vestibulopathy, especially if skew deviation and gaze-evoked nystagmus are negative Skew deviation - specific but not sensitive for central vestibular pseudoneuritis Gaze evoked nystagmus - supports central vestibular pseudoneuritis |
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Preventative agents for migraine.
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Nadolol
Amitriptyline Venlafaxine Verapamil Valproic acid Gabapentin Topiramate Botulinum neurotoxin A |
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Main features of PRES
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1. Confusion
2. Visual disturbances 3. Seizure 4. Headache |
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Poor prognostic indicators (physical exam or investigations) after CPR.
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1. No brain stem reflexes at any time.
2. Myoclonus status epilepticus within day 1. 3. Day 1-3 Somatosensory evoked potential absent N20 response. 4. Day 1-3 serum NSE (neuron specific enolase) > 33 mcg/L 5. Day 3 absent pupil, corneal reflex. Extensor or absent motor response. |
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Classic triad of findings in neurological Lyme disease
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1. Lymphocytic meningitis
2. Cranial neuritis 3. Radiculoneuritis |
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NCCT findings in acute ischemic stroke.
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1. Focal parenchymal hypodensity
2. Cortical swelling with sulcal effacement and loss of gray-white matter differentiation 3. Hyperdense MCA sign |
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What is the normal ratio of WBC:RBC in a traumatic tap?
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1:700
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What is CADASIL?
What are the main manifestations? |
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
Early onset of: 1. Ischemic episodes 2. Cognitive deficits 3. Migraine with aura 4. Psychiatric disturbances |
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Differential diagnosis of dementia.
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1. Alzheimer disease
2. Vascular dementia 3. Mixed AD/VaD 4. Dementia with Lewy Bodies 5. Parkinson's disease dementia 6. Fronto-Temporal Dementia |
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Classic features of Wernicke's encephalopathy.
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Encephalopathy
Oculomotor dysfunction Gait ataxia |
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If a patient's head is tilted one way, which eye does this suggest has a cranial nerve IV palsy?
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If head tilted left, then right eye likely has a CN IV palsy. Vice versa.
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Parinaud's syndrome: cause and signs associated with it.
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Pressure or infiltration of the tectum of the midbrain.
Impaired upgaze, fixed dilated pupils, non-reactive to light, but accommondation intact, Collier's sign (upper lid retraction causing widened palpebral fissure), convergence-retraction nystagmus |
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Clinical manifestation of top-of-the-basilar syndrome.
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1. Parinaud's syndrome.
2. Altered mental status (hypersomnolence, abulia, hallucinations, memory impairment). 3. Visual impairment. |
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What is locked-in syndrome?
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Infarction of base of the pons. Usually due to occlusive disease in proximal and middle segments of basilar artery.
Causes complete paralysis with sparing of consciousness, blinking and vertical eye movements. |
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What does dissemination in space mean in the MacDonald criteria for diagnosing MS?
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On MRI, one or more T2 lesions in at least two of four MS-typical regions of the CNS (periventricular, juxtacortical, infratentorial, or spinal cord) or by the development of a further clinical attack implicating a different central nervous system site. For patients with brainstem or spinal cord syndromes, symptomatic MRI lesions are excluded from the criteria and do not contribute to lesion count.
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What does dissemination in time mean in the MacDonald criteria for diagnosing MS?
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On MRI, the simultaneous presence of asymptomatic gadolinium-enhancing and nonenhancing lesions at any time, or a new T2 and/or gadolinium-enhancing lesion(s) on follow-up MRI, irrespective of its timing with reference to a baseline scan, or by the development of a second clinical attack
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