Neurology Flashcards
Outline the path taken by the corticospinal tract.
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.
What do alpha and gamma motor neurons innervate?
Alpha = skeletal muscles Gamma = muscle spindles
Explain how a muscle spindle works.
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.
What do muscle spindles sense?
What do golgi tendon organs sense?
Muscle spindles = LENGTH of MUSCLE
Golgi tendon organ = TENSION in MUSCLE
Explain the deep tendon reflex.
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.
Compare and contrast UMN and LMN lesions.
Weakness = BOTH Tone = UMN increased, LMN decreased Reflexes = UMN increased, LMN decreased Babinski = UMN upgoing, LMN downgoing Fasciculations = LMN Atrophy = greater in LMN
Explain the two main sensory pathways.
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.
What are the features of cauda-equina syndrome?
SYMPTOMS:
Back pain +/- radicular pain.
Bladder, bowel and sexual dysfunction.
SIGNS:
NEURO -
MOTOR: leg weakness, decreased reflexes
SENSORY: saddle anaesthesia, decreased anal tone
What are the features of Brown-Sequard syndrome?
IPSILATERAL LOSS = fine touch, proprioception and vibration
CONTRALATERAL LOSS = pain and temperature
What are bulbar and pseudobulbar palsies?
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.
How would you define delirium?
- 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
List common risk factors for delirium.
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)
What lab tests would you order is suspecting delirium?
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
Explain your approach to treating delirium.
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)
List 5 basic ADLs and 5 instrumental ADLs.
BASIC Able to: - Ambulate - Toilet - Shower - Dress - Feed INSTRUMENTAL - Manages finances - Manages transport - Manages medications - Manages meal preparation - Manages housecleaning
Explain the process of diagnosing Alzheimer’s disease.
- Screening test for cognitive impairment - e.g. RUDAS, MMSE, MoCA, Mini-Cog.
- History - assess for impairment in ADLs and IADLs (differentiates mild cognitive impairment from dementia).
- History of informant e.g. family member
- Neurological examination
- Investigations:
- Exclude reversible cause
- Routine IX in all patients with dementia:
FBC, EUC, BGL, TSH, Vit B12, folate
Brain imaging: MRI brain
What are the diagnostic criteria for dementia?
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.
What are the reversible causes/ mimics of dementia?
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
List the causes of dementia.
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
How would you treat Alzheimer’s disease?
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
ANTICHOLINESTERASES for ALZHEIMER’s DISEASE
- Commonly used drugs
- MOA
- UE
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
Explain the genetics of Alzheimer’s Disease.
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.
Explain the pathogenesis of Alzheimer’s Disease.
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.
What are Lewy Bodies? What conditions are they seen in?
Lewy Bodies are intracellular aggregates of alpha-synuclein (and other proteins e.g. ubiquitin).
Seen in Lewy Body Dementia and Parkinson’s Disease.