Neurology Flashcards

1
Q

Outline the path taken by the corticospinal tract.

A

UMN from the primary motor cortex in the precentral gyrus of the frontal lobe –>
descend via corona radiata and internal capsule –> brainstem –> at medulla, most fibers decussate at pyramids –> spinal cord as lateral corticospinal tract –> synapse with LMN in anterior horn.

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2
Q

What do alpha and gamma motor neurons innervate?

A
Alpha = skeletal muscles
Gamma = muscle spindles
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3
Q

Explain how a muscle spindle works.

A

When an alpha motor neuron fires, there is coactivation of gamma motor neurons –> so that when the skeletal muscle contracts, so do the intrafusal fibers = the muscle spindle retains its ability to sense changes in the muscle’s length despite movement.

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4
Q

What do muscle spindles sense?

What do golgi tendon organs sense?

A

Muscle spindles = LENGTH of MUSCLE

Golgi tendon organ = TENSION in MUSCLE

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5
Q

Explain the deep tendon reflex.

A

Tapping a large tendon with tendon hammer –> muscle spindle is stretched –> signal travels via Ia fibers –> afferents enter via dorsal root –> synapse with alpha motor neurons –> excitation –> activation of LMN –> muscle contraction.

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6
Q

Compare and contrast UMN and LMN lesions.

A
Weakness = BOTH
Tone = UMN increased, LMN decreased
Reflexes = UMN increased, LMN decreased
Babinski = UMN upgoing, LMN downgoing
Fasciculations = LMN 
Atrophy = greater in LMN
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7
Q

Explain the two main sensory pathways.

A

Dorsal column-Medial lemniscus pathway:
Carries fine touch, proprioception and vibration.
Enters via posterior root –> IPSILATERAL ascent in spinal cord –> synapse at medulla –> decussate –> synapse at thalamus –> somatosensory cortex.

Spinothalamic pathway:
Carries pain and temperature.
Enters via posterior root –> synapse –> decussate –> ascent in CONTRALATERAL spinal cord –> synapse at thalamus –> somatosensory cortex.

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8
Q

What are the features of cauda-equina syndrome?

A

SYMPTOMS:
Back pain +/- radicular pain.
Bladder, bowel and sexual dysfunction.

SIGNS:
NEURO -
MOTOR: leg weakness, decreased reflexes
SENSORY: saddle anaesthesia, decreased anal tone

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9
Q

What are the features of Brown-Sequard syndrome?

A

IPSILATERAL LOSS = fine touch, proprioception and vibration

CONTRALATERAL LOSS = pain and temperature

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10
Q

What are bulbar and pseudobulbar palsies?

A

BULBAR palsy = LMN lesion in brainstem motor nuclei controlling speech, mastication and swallowing.
PSEUDOBULBAR PALSY = UMN lesion to these same motor n.
CLINCIAL FX:
BOTH = problems with articulation, chewing and swallowing.
PSEUDOBULBAR = also emotional lability with uncontrollable crying/laughing etc.

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11
Q

How would you define delirium?

A
  • Primarily a disturbance of attention and awareness
  • May also have a change on cognition including: memory deficit, disorientation, perceptual disturbance e.g. hallucination
  • Develops rapidly and fluctuates over the day
  • Caused by a medical condition, intoxication or medication.
    Clinically, can be hypoactive, mixed, or hyperactive.
    HYPOACTIVE: sleeping, drowsy, lethargic
    HYPERACTIVE: agitated, labile mood
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12
Q

List common risk factors for delirium.

A
OLDER AGE
DRUGS
- Benzodiazepines
- Opioids
- Anticholinergics
- Antihistamines
- Corticosteroids
- Withdrawal e.g. alcohol
INFECTION
METABOLIC/ FLUIDS AND ELECTROLYTES
- CKD
- Liver failure
- PH abnormality
- Electrolyte abnormality
- Fluid overload or dehydration
INCREASED PHYSIOLOGICAL STRESS
- Surgical procedure
- Fever
- Pain
- Hypoxia or hypercarbia
- Hypoglycaemia
- Poor sleep
- Changed environment
- Retention: faecal or urinary
UNDERLYING BRAIN DISORDER
- Stroke
- Parkinson's
- MS
- Neoplasm
(consider 5 P's:
PEE - UTI, urinary retention
POO - constipation, impaction
PAIN
PUS - infection
POISION - medications, alcohol)
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13
Q

What lab tests would you order is suspecting delirium?

A
BEDSIDE:
Urinalysis, urine MCS
ECG
BLOODS:
FBC, EUC, LFTs, BGL, blood culture
CONSIDER: ABG, vitamin B12, folate, TSH, drug levels (e.g. digoxin, lithium), toxicology screen
IMAGING:
CXR
Consider head CT
Consider bladder scan
OTHER:
Consider LP
Consider EEG
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14
Q

Explain your approach to treating delirium.

A

First - prevent:
- Frequent reorientation
- Visits by family and friends encouraged
- Good sleep - quiet room, minimize interruptions at night
- Early mobilization and rehabilitation
- Visual and hearing aids
- Adequate hydration and food
Once established:
- Reverse any treatable cause - e.g. IV fluids for dehydration, antibiotics for infection
- Ensure patient has their visual and hearing aids
- Frequent reorientation by staff, provide time and location cues e.g. clock, calendar
- Quiet, restful environment
- Medication reconciliation, eliminate any unnecessary medications
AVOID:
- Physical restraints
- Routine use of antipsychotics - only use if severe symptoms that are distressing and dangerous for patient - haloperidol - be aware of QT prolongation.
- Do not use benzodiazepines (only if alcohol withdrawal is the cause)

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15
Q

List 5 basic ADLs and 5 instrumental ADLs.

A
BASIC
Able to:
- Ambulate
- Toilet
- Shower
- Dress
- Feed
INSTRUMENTAL
- Manages finances
- Manages transport
- Manages medications
- Manages meal preparation
- Manages housecleaning
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16
Q

Explain the process of diagnosing Alzheimer’s disease.

A
  1. Screening test for cognitive impairment - e.g. RUDAS, MMSE, MoCA, Mini-Cog.
  2. History - assess for impairment in ADLs and IADLs (differentiates mild cognitive impairment from dementia).
  3. History of informant e.g. family member
  4. Neurological examination
  5. Investigations:
    - Exclude reversible cause
    - Routine IX in all patients with dementia:
    FBC, EUC, BGL, TSH, Vit B12, folate
    Brain imaging: MRI brain
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17
Q

What are the diagnostic criteria for dementia?

A
Significant decline in performance
in 1 (or more) cognitive domain:
- Memory and learning
- Executive functioning
- Visuo-spatial
- Language
- Personality, behaviour
- Praxis
These impair functioning in everyday activities.
18
Q

What are the reversible causes/ mimics of dementia?

A

DEMENTIAS
Drugs –> medication reconciliation
Eyes and ears –> ensure patient has glasses and hearing aids
Metabolic:
Hypo/hyper Na, Ca –> EUC&CMP and correct
Hypothyroidism –> TSH and thyroid hormones
Vitamin B12 deficiency –> B12 level and replacement
Epilepsy –> consider EEG
Emotion –> depression –> history to determine mood
Normal pressure hydrocephalus (wacky, wobbly and wet) –> Brain CT
Tumour (space occupying lesion - CNS tumour, intracranial bleed) –> Brain CT
Infection –> FBC, CRP, HIV and syphilis testing, LP
AF, Alcohol –> ECG, alcohol history
Sleep apnoea –> Sleep study

19
Q

List the causes of dementia.

A
NEURODEGENERATIVE DISEASE
- Alzheimer
- Dementia with Lewy Bodies
- Parkinson's disease
- Frontotemporal dementia
CNS INFECTION
- HIV
- Neurosyphilis
CEREBROVASCULAR
- Vascular dementia
HEAD INJURY
- Traumatic brain injury
- Dementia pugilistica
NORMAL PRESSURE HYDROCEPHALUS
PRION DISEASE
- Creutzfeldt-Jakob disease
- Kuru
20
Q

How would you treat Alzheimer’s disease?

A

LIFESTYLE

  • Exercise
  • Social activities
  • Cognitive stimulation
  • Medication reconciliation - avoid unnecessary medication esp. those with anticholinergic properties

PHARMACOLOGY
Mild/moderate AD –>
- Cholinesterase inhibitor: stabilises cognitive and global functioning for approx. 6-12 months, but then function generally declines.
- Vitamin E
Severe AD –>
- Cholinesterase inhibitor may be effective
- Memantine (NMDA receptor antagonist - reduce glutamate-mediated neurotoxicity) can be used in severe disease

MONITORING
- Regular monitoring: for disease progression, comorbidities (e.g. depression) and medication UE

ADVANCE CARE PLANNING

CONSIDER WELLBEING OF CAREGIVER
- Respite care

21
Q

ANTICHOLINESTERASES for ALZHEIMER’s DISEASE

  • Commonly used drugs
  • MOA
  • UE
A
Donepezil, Galantamine, Rivastigmine
MOA: inhibit cholinesterase enzyme --> reduce breakdown of acetylcholine 
UE: cholinergic effects -->
- Bradycardia
- Miosis 
- N&V, diarrhoea, abdominal pain
- Urinary incontinence
- Hypersalivation
- Sweating
- Insomnia or drowsiness, vivid dreams
22
Q

Explain the genetics of Alzheimer’s Disease.

A

Most cases are sporadic.
Familial and autosomal dominant cases can occur.
Autosomal dominant - causes early onset AD
- APP gene on chromosome 21 (excess APP leads to cerebral amyloid production)
- Presenilin 1 (most common cause of inherited AD) & - Presenilin 2 (affect cleavage of APP)
Familial late onset AD
- APO-E gene
There are three APOE types - E2, E3 and E4.
APOE4 brings the greatest risk: 1 allele increases risk 2-3x, 2 alleles increase risk 10x.

23
Q

Explain the pathogenesis of Alzheimer’s Disease.

A

TAU:
- Tau stabilizes microtubules
- In AD, tau is hyperphosphorylated –> microtubule dysfunction & tau aggregation into neurofibrillary tangles (intracellular)
BETA-AMYLOID:
- Amyloid precursor protein (APP). Beta-amyloid is cleaved from APP by secretases. Cleavage by Beta or Gamma secretases can produce Beta-amyloid 40 or 42. In AP, there is an abnormal increase in B-amyloid-42, which forms (1) neurotoxic oligomers, and (2) Amyloid plaques (extracellular).

Neurofibrillary tangles and amyloid plaques –> neurotoxic (loss of neurons, brain atrophy), altered neurotransmitter signalling esp. acetylcholine.

24
Q

What are Lewy Bodies? What conditions are they seen in?

A

Lewy Bodies are intracellular aggregates of alpha-synuclein (and other proteins e.g. ubiquitin).

Seen in Lewy Body Dementia and Parkinson’s Disease.

25
Q

MAO-Inhibitors.
Types and their uses.
Indications.
UE.

A

MAOI
- Non-selective inhibitors of monoamine oxidase –> decrease breakdown of adrenaline, NA, serotonin and dopamine.
Used for depression.

  • Selective MAO-B inhibitor - selegiline. Mainly inhibits breakdown of dopamine –> increased dopamine level.
    Used for Parkinson’s disease.

The major UE is a hypertensive crisis.
Ingestion of foods containing TYRAMINE (cheese, cured meats, beer) when MAO is inhibited –> tyramine entry into systemic circulation –> stimulation of SNS –> hypertensive crisis.

Risk of serotonin syndrome if used with other serotonergic drugs - e.g. SSRI, SNRI, TCAs, St John’s Wort.

Serotonin Syndrome:
Classic triad is:
1. Neuromuscular excitability –> hyper-reflexia, hypertonia, myoclonus, tremor
2. Autonomic dysfunction –> tachycardia, tachypnoea, hyperthermia, HTN, sweating, diarrhoea
3. Altered mental status –> agitation, coma

26
Q

MEDICATIONS FOR PARKINSON’S DISEASE
Common medications and how they are used in combination
MOAs
UEs of anti-Parkinson medications

A

L-DOPA:
MOA: converted to dopamine by DOPA decarboxylase at the presynaptic neuron –> increased dopamine acting on receptors.
Usually first-line, especially in older patients > 65 years

CARBIDOPA: DOPA decarboxylase inhibitor
MOA: prevents peripheral conversion of L-DOPA to dopamine –> increased L-DOPA reaching brain and decreased peripheral dopamine = decreased UE.

DOPAMINE AGONISTS: pramipexole, cabergoline, pergolide, ropinirole, bromocriptine
MOA: act on dopamine receptors in the striatum –> increased dopaminergic effect
Often used in younger patients

COMT INHIBITORS: entacapone, tolcapone
MOA: inhibition of COMT enzyme (breaks down L-DOPA into 3-MT) in the periphery (and tolcapone also acts in CNS) –> increased L-DOPA –> increased dopaminergic effect.
Uses: in combination with L-DOPA and carbidopa for refractory PD and if on-off effect problematic.

MAO-B INHIBITORS: selegiline
MOA: inhibition of MAO-B enzyme (breaks down L-DOPA to DOPAC) in the CNS –> increased L-DOPA

ACH MUSCARINIC ANTAGONISTS: block overactivity of muscarinic acetylcholine receptors

AMANTADINE: NMDA receptor antagonists - block neurotoxic effect of excess glutamate

UE and RISKS with Anti-Parkinson’s medication:

  • On-off effect (periods of good function alternating with poor function as L-DOPA wears off)
  • Dystonia/ dyskinesia (abnormal tone and movements)
  • Impulse-control disorders: especially with dopamine agonists - e.g. pathological gambling, hypersexuality
  • Drug-induced psychosis
27
Q

What are the clinical features of Parkinson’s Disease?

A

TRIAD:

  1. Bradykinesia
  2. Tremor - asymmetrical, resting, pill-rolling
  3. Rigidity - lead pipe or cogwheeling
PRODROMAL:
Constipation
Anosmia
REM sleep disorder
Psychiatric - e.g. mood changes
OTHER FEATURES:
Gait - shuffling, small steps, festination, slow turns, freezing, reduced arm swing
Postural instability --> falls
Autonomic dysfunction --> bladder and bowel dysfunction (constipation, urinary retention, incontinence), orthostatic hypotension
Mask-like facies
Primitive reflexes - glabellar tap
Stooped posture
Micrographia
28
Q

List contraindications to LP.

A

Signs of increased ICP - e.g. focal neurologic signs, papilloedema, markedly reduced LOC (<8)

Space occupying intracranial mass

Uncontrolled bleeding diathesis

Local overlying skin infection

Unstable patient

29
Q

What are the possible UE/ risks of a LP?

A

Local discomfort

Headache

Failure to obtain CSF (dry tap)

Bleeding - traumatic tap, spinal haematoma

Neurological - nerve damage (should not occur if performed correctly), brainstem herniation

Infection

30
Q

Explain the procedure of LP.

A
  • Informed consent
  • Positioning - lying on side or sitting up; back curved
  • Measure from top of iliac crests, which are at level of L3/4 interspace –> go into this level or 1 below (spinal cord stops at L1/2 level)
  • Prepare: sterile field, skin
  • Local anaesthetic
  • Insert needle and advance until resistance gives
  • Remove stylet and collect CSF into 3 tubes (5-10 drops/tube)
  • Remove needle
  • Apply dressing
  • Document
  • Monitor
31
Q

When might you order a CT before LP?

A
Signs of raised ICP
Known CNS disease
Suspected SAH
Seizure in past 1 week
Age > 60 years
Immunocompromise
32
Q

What tests would you order on CSF if suspecting meningitis?

Compare expected results in viral and bacterial meningitis.

A
Test for:
WBC
RBC
Protein
Glucose
CSF pressure
MCS
VIRAL:
WBC 5-1,000; lymphocytes
Protein increased +
Normal glucose
Normal CSF pressure
Negative gram stain and culture
BACTERIAL:
WBC 1,000+; PMNs
Protein increased +++
Decreased glucose
Increased CSF pressure
Positive gram stain and culture
33
Q

What are the common pathogens that cause bacterial meningitis?

A

Strep pneumoniae
N meningitidis
Haemophilus influenzae type b

+ possibly consider
Neonates – GBS and E coli
Neurosurgery or penetrating injury – S aureus

34
Q

What is your approach to suspected bacterial meningitis?

A

Rapid assessment with concurrent hx, examination and investigation and treatment. NO IX should delay the administration of IV ABX if bacterial meningitis is suspected.

Bedside: LP
Labs: FBC, EUC, LFTs, CRP, BGL (blood glucose used to interpret CSF glucose), blood culture (at least 2 sets from different sites), VBG (lactate), coags (may contraindicate LP, but do not wait for results before LP unless coagulopathy likely)
Imaging: in some patients, CT brain is required before LP

Treatment:

  • Admit
  • Consult: ID + neurology
  • Immediate empiric IV ABX plus dexamethasone (must be given before or concurrent with ABX for best effect)
  • Swap to targeted ABX when results of MCS known
  • Supportive care:
  • – IV cannula + IV fluids
  • – Raise head if raised ICP
  • – Monitor: for sepsis
  • Infection control measures - droplet precautions
  • Chemoprophylaxis for close contacts of patients with N meningitidis and HIB
  • Report to public health
  • Audiometry
35
Q

What are the complications of bacterial meningitis - acute and long term?

A

ACUTE:

  • Seizure
  • Septic shock
  • ARDS and respiratory failure
  • DIC
  • SIADH
  • Brain abscess

CHRONIC:

  • Sensorineural deafness
  • Blindness
  • Weakness
  • Ataxia
  • Cognitive impairment
36
Q

List risk factors for meningitis.

A
  • Age: very young (< 5 years) or very old (>65 years)
  • Immunocompromise: HIV, steroids, asplenic
  • Not immunized
  • Recent infection: URTI, sinusitis, otitis, mastoiditis
  • Head trauma
  • Neurosurgery
  • Crowded living conditions
  • Close contact with infected person
37
Q

What are the common pathogens causing viral meningitis?

A

Enteroviruses (most common!!)
HSV, CMV, EBV, VZV
Measles
Mumps

38
Q

List the clinical features of acute meningitis.

A

TRIAD is: (1) fever, (2) headache, (3) neck stiffness

VITAL SIGNS: fever, tachycardia, possibly hypotension (septic shock)
SYSTEMIC:
- malaise
- rash: non-blanching purpura in N meningitidis
- N&V
NEUROLOGICAL:
- Headache
- Neck stiffness
- Kernig sign (lying supine with hip flexed to 90 –> passive knee extension is resisted)
- Brudzinski sign (lying supine and passively flex neck –> hip/ knee flexion)
- Photophobia
- Papilloedema

FX that suggest encephalitis:

  • Altered LOC
  • Seizures
  • Focal neurological signs
39
Q

How would you treat viral meningitis/encephalitis?

A

Same as for bacterial meningitis, but acyclovir instead of ABX.

Rapid assessment with concurrent hx, examination and investigation and treatment. NO IX should delay the administration of IV ABX if bacterial meningitis is suspected.

Bedside: LP
Labs: FBC, EUC, LFTs, CRP, BGL (blood glucose used to interpret CSF glucose), blood culture (at least 2 sets from different sites), VBG (lactate), coags (may contraindicate LP, but do not wait for results before LP unless coagulopathy likely)
Imaging: in some patients, CT brain is required before LP

Treatment:

  • Admit
  • Consult: ID + neurology
  • Acyclovir
  • Supportive care:
  • – IV cannula + IV fluids
  • – Raise head if raised ICP
  • – Monitor: for sepsis
  • Infection control measures - droplet precautions
  • Audiometry
40
Q

What are the clinical features of Motor Neuron Disease?

A
BOTH UMN and LMN signs.
Bulbar and pseudobulbar signs - 
- Dysarthria
- Dysphagia
- Involuntary inappropriate laughing/ crying
41
Q

Explain EMG and nerve conduction studies.

A

EMG - stimulate a peripheral nerve and measure the action potentials in associated muscle.

Nerve conduction studies - stimulate a nerve (motor or sensory) at 2 points and measure the conduction velocity and amplitude of the action potential