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Neurological Conditions Flashcards

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1
Q

MULTIPLE SCLEROSIS

  1. What is Multiple Sclerosis?
  2. What is the pathophysiology of Multiple Sclerosis?
  3. What is the Epidemiology of Multiple Sclerosis?
  4. What are the associations of Multiple Sclerosis?
  5. What are the four clinical patterns of Multiple Sclerosis?
  6. What are differential diagnoses of Multiple Sclerosis?
  7. What is the triad associated with Multiple Sclerosis? What does it comprise of?
  8. What investigations can be ordered to confirm Multiple Sclerosis? What is seen with these investigations?
  9. What are Dawson fingers? What are they associated with?
  10. What criteria is used to help diagnose Multiple Sclerosis? Simplify what this criteria is?
  11. If a patient only has 1 singular attack of symptoms, is this enough to diagnose Multiple Sclerosis?
  12. If a patient only has 1 attack as seen radiologically, is this enough to diagnose Multiple Sclerosis?
  13. What is the most common presenting feature of Multiple Sclerosis? What are other features?
  14. What is the management of Multiple Sclerosis during relapse?
  15. What is the management of Multiple Sclerosis SYMPTOMS?
  16. Give examples of drugs being used to prevent relapses of Multiple Sclerosis?
A
  1. An idiopathic, autoimmune disease of the central nervous system. Characterised by demyelination and axonal loss is discrete areas called plaques
    • Type 4 Hypersensitivity reaction: T-Cell Mediated Immune Response
  3. Demyelination → Destruction of myelin and oligodendrocytes
  4. Acute Inflammation around demyelinated regions
  5. Plaque formation after incomplete healing
    - Earlier on, may get re-myelination however later it may become irreversible
    • 3x more common in women than in men
      - Most commonly diagnosed from 20-40 years old
    • Westernisation / Viking countries
      - Higher latitudes of world / Low Vit D
      - Epstein-Barr virus
      - Smoking
      - Obesity
    • Relapsing-remitting - most common
      - Primary progressive
      - Secondary progressive
      - Progressive relapsing
    • Neurosarcoidosis
      - Neuromyelitis Optica
      - Vasculitides
  10. Charcot’s Neurological Triad
  11. Nystagmus
  12. Dysarthria
  13. Intention tremor
    1. MRI: T2 White matter plaques which are well-defined, homogenous, ovoid - especially in corpus callosum, periventricular regions, brain stem, peduncles
  15. CSF: Oligoclonal bands of IgG
  16. Evoked potentials: Decreased velocity
  17. Hyperintense lesions penpendicular to the corpus callosum, specific for Multiple Sclerosis
  18. McDonald’s Criteria, attacks / lesions must be spread over space and time
  19. No, it is a clinically isolated syndrome (CIS)
  20. No, it is a radiologically isolated syndrome (RIS)
    • Optic neuritis: acute vision loss, painful eye movements, diplopia, impaired colour vision, reduced visual acuity, Marcus Gunn pupil (relative afferent pupillary defect)
  • Motor symptoms → Hypertonia, hyperreflexia, spastic weakness
  • Uhthoff’s phenomenon → Worsening of vision following rise in body temperature
  • Lhermitte’s phenomenon → Electric shock-like sensation on flexion of neck
  • Cerebellar → Ataxia
  • Other → Urinary incontinence, sexual dysfunction, intellectual deterioration
    • 3-5 day course of oral / IV methylprednisolone to shorten length of relapse
      - It does not decrease severity of symptoms
    • Spasticity / Contractions: Baclofen, Gabapentin, Benzos, Botox
    • Fatigue: Amantadine, Modafine
    • Bladder dysfunction: Oxybutynin, Botox
    • Depression: SSRIs
    • Alemtuzimab
      - Beta-inferferon
      - Dimethylfumarate
      - Fingolimod
      - Natalizumab
      - Teriflunomide
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2
Q

MOTOR NEURONE DISEASE

  1. What is Motor Neurone Disease (MND)?
  2. What is the epidemiology of Motor Neurone Disease (MND)?
  3. What are some associations with MND?
  4. What is the overall prognosis of MND?
A
  1. An umbrella term for progressive, ultimately fatal conditions of unknown cause where the motor neurones stop functioning. Presents with both upper (cortex → spine) and lower motor neuron signs (spine → muscle)
  2. Rarely presents before the age of 40
  3. Genetics / FHx, Smoking, Exposure to heavy metals, Certain pesticides
  4. 50% die within 3 years
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3
Q

MOTOR NEURONE DISEASE

What are the subtypes of Motor Neurone Disease (MND)?

A
  1. Amyotrophic Lateral Sclerosis (ALS)
  2. Primary Lateral Sclerosis (PLS)
  3. Progressive Muscular Atrophy (PMA)
  4. Progressive Bulbar Palsy (PBP)
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4
Q

MOTOR NEURONE DISEASE

What is the most common and second most common subtype of Motor Neurone Disease?

Which subtypes of Motor Neurone Disease have the best and worst prognosis?

A

Amyotrophic Lateral Sclerosis - most common
Progressive Bulbar Palsy - 2nd most common

Progressive Muscular Atrophy - best prognosis
Progressive Bulbar Palsy - worst prognosis

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5
Q

MOTOR NEURONE DISEASE

What is the management of Motor Neurone Disease (MND)?

A
  • Riluzole
    • Prevents stimulation of glutamate receptors
    • Used mainly in amyotrophic lateral sclerosis
    • Prolongs life by about 3 months
  • Respiratory care
    • Non-invasive ventilation (usually BIPAP) is used at night. Studies have shown a survival benefit of around 7 months
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6
Q

MOTOR NEURONE DISEASE

For all the subtypes of MND, what motor neurones are affected?

A

Amyotrophic Lateral Sclerosis: UMN & LMN
Primary Lateral Sclerosis: UMN only
Progressive Muscular Atrophy: LMN only
Progressive Bulbar Palsy: UMN & LMN

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7
Q

Outline the presentation of Progressive Bulbar Palsy?

A

Palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei

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8
Q

MOTOR NEURONE DISEASE

What are some features of Motor Neuron Disease?

A
  • Fasciculations
  • Absence of sensory signs/symptoms
  • Mixture of lower motor neuron and upper motor neuron signs
  • Wasting of the small hand muscles/tibialis anterior is common
  • Doesn’t affect external ocular muscles
  • No cerebellar signs
  • Abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
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9
Q

BRAINSTEM DEATH

How is Brainstem death assessed?

A

6 Reflexes are tested:
1. Pupillary reflex (no response to sharp changes in light intensity)

  1. Corneal reflex (no reflex on stimulating cornea by touch or foreign body)
  2. Oculovestibular reflex (aka caloric test, no eye movements on pouring 50ml ice cold water into each ear)
  3. Cough reflex (no reflex to bronchial stimulation or gag on pharyngeal stimulation)
  4. Absent response to supraorbital pressure
  5. No respiratory effort (when disconnecting ventilator for long enough i.e. at least 5mins to ensure paCO2 >6 kPA)
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10
Q

BRAINSTEM DEATH

What professionals can assess brainstem death?

A
  • Must be completed by two doctors on two separate occasions
  • Both must be experienced in brain stem tests
  • Must be >5 years postgrad experience
  • 1 must be a consultant
  • Cannot be a member of transplant team if patient will be harvested
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11
Q

IDIOPATHIC INTRACRANIAL HYPERTENSION

What are the risk factors for Idiopathic Intracranial Hypertension?

What are the features of Idiopathic Intracranial Hypertension?

What are some management of Idiopathic Intracranial Hypertension?

A
  • Female, Obesity, Pregnancy, Drugs: COCP, Vit A, Tetracyclines, Lithium
  • Headache, Blurred vision, Papillo-oedema, Enlarged blind spot, CN6 palsy
  • Weight loss, Diuretics → Acetazolamide, Topiramate, Repeated lumbar punctures, Surgery → Optic nerve sheath decompression
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12
Q

TREMOR

  1. What is a tremor?
  2. What are the three main types?
  3. Describe a resting tremor, example?
  4. Describe a postural tremor, example?
  5. Describe an intention tremor, example?
A
  1. Involuntary, rhythmic oscillations or movements of part of the body
  2. Postural Tremor, Resting Tremor, Intention Tremor
  3. Low frequency, worse with rest, eases with activity. Example → Parkinsonism, “pill-rolling”
  4. Worse on certain postures, i.e. putting hands out. Examples → As seen in Salbutamol use, Hyperthyroidism, Hepatic encephalopathy
  5. Worse with intention movements. Example → As seen in cerebellar causes
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13
Q

TREMOR

  1. Describe a Benign Essential Tremor?
  2. When do Benign Essential Tremors get better or worse?
  3. How can you manage a Benign Essential Tremor?
A

Benign Essential Tremor is a form of postural tremor. It is a fine, symmetrical tremor more noticeable on voluntary movements. Typically affects the upper body; classically hands but also head, jaw and voice

Get better with sleep, due to paralysis of the voluntary muscles and alcohol. Gets worse with tiredness, stress, caffeine

Propanolol beta-blocker. Primidone barbiturate anti-epileptic. ?Referral to neurology to rule out other causes

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14
Q

FACIAL NERVE PALSY

  1. What cranial nerve is the Facial Nerve?
  2. What is the motor function of the Facial Nerve?
  3. What is the sensory function of the Facial Nerve?
  4. What is the parasympathetic function of the Facial Nerve?
  5. What are the five terminal branches of the Facial Nerve?
  6. Is the facial nerve an Upper or Lower Motor Neuron?
A
  1. CN7
  2. Muscles of facial expression, stapedius in inner ear, posterior digastric, stylohyoid and platysma
  3. Anterior 2/3rds of tongue
  4. Supply to submandibular and sublingual salivary glands and lacrimal gland
  5. Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical
  6. Lower Motor Neuron
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15
Q

FACIAL NERVE PALSY

  1. What is Bell’s Palsy?
  2. What is it thought to be associated with?
  3. In what age group is it commonly seen in?
  4. What are the clinical features of Bell’s Palsy and why?
A
  1. An acute, unilateral, idiopathic facial nerve paralysis with unknown aetiology
  2. Associated with concurrent viral infection (HSV-1, CMV, EBV), diabetes, pregnancy
  3. 20-40 year olds
  4. Unilateral weakness of facial muscles (from forehead to chin) - due to LMN facial nerve palsy, inability to close the eye - due to temporal and zygomatic branches of facial nerve, metallic taste - due to chorda tympani, hyperacusis - due to stapedius nerve, reduced lacrimation - due to greater petrosal nerve
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16
Q

FACIAL NERVE PALSY

  1. What is the classification of Bell’s Palsy severity?
  2. What are differentials to LMN causes of unilateral facial weakness?
  3. How is Bell’s Palsy diagnosed?
  4. How is Bell’s Palsy managed?
  5. What is the prognosis of Bell’s Palsy?
  6. What are poor prognostic factors of Bell’s Palsy?
A
  1. House-Brackmann classification
  2. Infective (acute otitis media, cholesteatoma, viral infection HSV-1, CMV, EBV), Neoplasm (parotid tumour), Trauma, Ramsay-Hunt syndrome (due to herpes zoster), acoustic neuroma, parotid tumours, HIV, multiple sclerosis*, diabetes mellitus
  3. Clinical diagnosis, Serology for HSV-1, VZV - however management plan may not change
  4. Eye care → hourly lubricating drops or eye patch, If < 72 hours presentation, oral steroids indicated, 25 mg BD for 10 days or 60 mg BD for 5 days plus daily reduction dose by 10mg for 5 days. Antiviral use is controversial
  5. 85% make a full recovery, which can take upto 12 months. The remainder may be left with residual symptoms
  6. Having complete palsy, No signs of recovery after 3 weeks, Associated pain, Ramsay Hunt syndrome, Age >60 years old, HTN, DM, pregnancy
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17
Q

FACIAL NERVE PALSY

  1. Why is there sparing of the forehead in an UMN lesion causing facial paralysis?
  2. If an UMN lesion occurs and there is unilateral facial weakness, what are your differentials?
  3. If an UMN lesion occurs and there is bilateral facial weakness, what are your differentials?
A
  1. Due to bilateral innervation of the forehead muscle
  2. CVA, tumour, subdural haematoma
  3. Pseudobulbar palsy, motor neurone disease
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18
Q

NEUROPATHIC PAIN

  1. What is Neuropathic Pain and what is it caused by?
  2. What are some causes of Neuropathic Pain?
  3. What are the typical features of Neuropathic Pain?
  4. What can be used to help diagnose Neuropathic Pain?
  5. What is the first-line management of Neuropathic Pain?
  6. Aside from first-line management, what else can be used for Neuropathic Pain?
  7. What is the exception to the rule in the first-line management of Neuropathic Pain?
A
  1. A type of pain characterised by abnormal functioning of sensory nerves delivering abnormal and painful signals to the brain
  2. Postherpetic neuralgia from shingles (dermatomal distribution, usually on trunk), Nerve damage from surgery, Multiple Sclerosis, Diabetic neuropathy affecting feet, Trigeminal neuralgia, Complex Regional Pain Syndrome (CRPS)
  3. Burning, Tingling, Pins and needles, Electric shocks, Loss of sensation to touch of affected area
  4. DM4 Questionnaire, must have at least 4/10 for their pain
  5. Amytryptilline, Duloxetine, Gabapentin, Pregabalin
    • Tramadol opioid, only for short-term control of flares
    • Capsaicin cream, for localised areas of pain
    • Physiotherapy to maintain strength
    • Psychological input
  7. Carbamazepine for Trigeminal Neuralgia
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19
Q

HUNTINGTON’S DISEASE

  1. What is Huntington’s Disease?
  2. What is the inheritance pattern of Huntington’s Disease?
  3. What is the epidemiology of Huntington’s Disease?
  4. Outline the pathophysiology of Huntington’s Disease
  5. What happens if a patient does not have >36 CAG repeats?
  6. What is the relation between CAG repeats and penetrance in Huntington’s Disease?
  7. Outline the process of genetic anticipation of Huntington’s Disease
  8. In what sets of patients does genetic anticipation of Huntington’s Disease more frequently occur
  9. What are the clinical features of Huntington’s Disease?
  10. What is the management of Huntington’s Disease?
  11. What is the prognosis for Huntington’s Disease?
A
  1. A rare progressive, neurodegenerative disease, caused by a trinucleotide expansion repeat of the Huntington gene on chromosome 4
  2. Autosomal dominant
  3. Age of presentation is approx 40, however this can be variable due to anticipation
  4. Trinucleotide expansion repeat of CAG, >36 repeats. This causes abnormal Glutamine levels to build up in the caudate and putamen of the basal ganglia, causing neuronal death. This can lead to disorders of cognition, movement and mood
  5. If they have between 27 - 35, they are considered premutation alleles. They do not have the disease however increased risk to their offspring
  6. If between 36-39 → variable penetrance. If >40 → full penetrance
  7. The trinucleotide expansion repeats of CAG can be misread by DNA polymerase, causing further CAGs to be inserted. The more repeats, the earlier the age of onset in the next generation of the patient
  8. Men
    • Chorea → dance-like, involuntary, abnormal movements
    • Athetosis → slow, snake like movements
    • Personality changes, i.e. depression
    • Saccadic eye movements
    • Dysarthria, dysphagia
    • No cure, symptomatic relief
      - Antipsychotics (e.g. olanzapine)
      - Benzodiazepines (e.g. diazepam)
      - Dopamine-depleting agents (e.g. tetrabenazine)
    • 10-20 years from diagnosis, due to aspiration pneumonia
      - Increased risk of suicide
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20
Q

COMPLEX REGIONAL PAIN SYNDROME

  1. What is Complex Regional Pain Syndrome?
  2. What is the presentation?
  3. What is the management?
A
  1. Neuropathic pain, usually isolated to one limb. Often triggered by injury to that area
  2. Area can become painful, hypersensitive even to simple inputs such as wearing clothing. Can also intermittently swell, change colour, change temperature, flush with blood and have abnormal sweating
  3. Physiotherapy, neuropathic analgesics, refer to pain clinic
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21
Q

PARKINSON’S DISEASE

  1. What is Parkinson’s Disease?
  2. What is the epidemiology of Parkinson’s Disease?
  3. What is the substantia nigra? What is its function and how is it affected in Parkinson’s Disease?
  4. What is the classic triad of Parkinson’s Disease?
  5. Describe the tremor in Parkinson’s Disease?
  6. How does a Parkinsonian tremor compare to a Benign Essential Tremor?
  7. Outline what “Cogwheeling” is?
  8. Outline how a PD patient may demonstrate Bradykinesia?
  9. What are other features of Parkinson’s Disease, outside the typical triad?
  10. How may drug-induced Parkinsonism present compared to PD? What medications may cause drug-induced Parkinsonism?
  11. How is Parkinson’s Disease diagnosed?
  12. What is the first-line management of Parkinson’s Disease?
A
  1. Parkinson’s Disease is a progressive, neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra of the basal ganglia.
  2. Second most common neurodegenerative condition after Alzheimer’s Disease. Increases with age, commonly after 70. More common in males than females
  3. The substantia nigra is a part of the basal ganglia. It controls movement via the motor cortex. It is divided into the pars compacta and the pars fasciculata. Ie nin Parkinson’s Disease, the pars compacta is affected, preventing transmission via the nigrostriatal pathway
  4. Resting tremor (classically asymmetrical), Rigidity, Bradykinesia
  5. Unilateral, asymmetrical tremor, 4-6 Hz in frequency, “Pill rolling”, Worse at rest, and improves on moving
  6. A Benign Essential Tremor is 5-7 Hz in frequency, whereas a PD tremor is 4-6 Hz. A BET also is symmetrical, whereas a PD one is not. BET also improves with rest, whereas a PD tremor does not. A BET also improves with alcohol, whereas a PD one does not.
  7. Resistance to passive movement of a joint. Hand on passive flexion and extension will demonstrate tension (cogwheeling)
  8. Movements become slower and smaller, i.e. Handwriting (micrographia), Shuffling gait, Reduced facial expressions, mask-like (hypomimia)
    • Drooling of saliva
      - Anosmia (loss of sense of smell)
      - Postural hypotension due to autonomic failure
      - Postural instability
      - Depression
      - REM disturbance (sleep disturbances, insomnia)
      - Cognitive impairment
  10. Features may be slightly different
    Symptoms tend to have rapid onset and are bilateral
    Rigidity and resting tremor are UNCOMMON. Typical and Atypical antipsychotics, i.e. Chlorpromazine, Prochlorperazine, Antiemetics, i.e. Metoclopramide
  11. Mainly, a clinical diagnosis
    - Can use PD UK Society Brain Bank Clinical Diagnostic Criteria
    - May want to consider SPECT
    • If motor symptoms affect QoL → Levodopa
      - If motor symptoms do not affect QoL → Dopamine agonists, Levodopa or MAO-B Inhibitor
22
Q
  1. What are the four Parkinson-Plus Syndromes?
  2. Outline what Multiple System Atrophy is?
  3. Outline what Dementia with Lewy Body is?
  4. Outline what Progressive Supranuclear Palsy is?
A
  1. Multiple System Atrophy (MSA), Dementia with Lewy Body (DLB), Progressive Supranuclear Palsy (PSP), Corticobasal Degeneration (CBD)
  2. A Parkinson-Plus Syndrome, Two main types: MSA-P, MSA-C, Parkinsonism + autonomic disturbances: erectile dysfunction, postural hypotension, atonic bladder, constipation, abnormal sweating, cerebellar signs
  3. A type of Parkinson-Plus Syndrome, Cognitive symptoms develop within a year of Parkinsonism, whereas with PD with dementia, cognitive symptoms develop much later
  4. A type of Parkinson-Pulse Syndrome, impairment of vertical gaze (upward gaze > downward gaze), Will have difficulty reading or descending stairs
23
Q
  1. Outline the pharmacology of Levodopa? How effective is it?
  2. What are dyskinesias seen in Levodopa?
  3. How is Levodopa taken?
  4. If a patient is NBM, how can they take their Levodopa medication?
A
  1. Synthetic Dopamine precursor. Only effective for 5-10 years until dyskinesias occur
  2. Excessive motor activity → Dystonia, chorea, athetosis
  3. Doesn’t usually cross the BBB, must be given with peripheral decarboxylase inhibitors
    - Levodopa + Carbidopa → Co-careldopa
    - Levodopa + Benserazide → Co-benyldopa
  4. Can take a rescue medication patch → Rotigotine
24
Q
  1. Give examples of Dopamine agonists used in PD?

2. What are some complications of Dopamine agonist use?

A
  1. Bromocriptine, Ropinirole, Cabergoline, Apomorphine
  2. Can cause pulmonary, retroperitoneal and cardiac fibrosis → Echo, ESR, Creatinine, CXR as baseline. Can cause impulse control disorders → patient counselling and education
25
Q

TRIGEMINAL NEURALGIA

  1. What is Trigeminal Neuralgia? What is it caused by?
  2. What are the features of Trigeminal Neuralgia?
  3. How is Trigeminal Neuralgia managed?
  4. What are the red flag features of Trigeminal Neuralgia?
A
  1. A pain syndrome of severe, unilateral pain. Can be an unknown cause, or due to trigeminal root compression by tumour or vascular problems
  2. Unilateral, brief, electric shock pains, Abrupt in onset and termination, Caused by light touch such as combing, washing, shaving, using toothbrush, Small areas such as nasolabial folds are susceptible
  3. First line: Carbamazepine. Failure to respond or red flag features → Neuro referral
  4. Sensory changes, Deafness or other ear problems, History of skin or oral lesions spreading perineurally, Optic neuritis, Family history of Multiple Sclerosis, Age of onset < 40 years, Pain only in Ophthalmic branch of Trigeminal nerve
26
Q

TEMPORAL ARTERITIS

  1. What is Temporal Arteritis?
  2. What are some features of Temporal Arteritis?
  3. What are some investigations of Temporal Arteritis? What may the results be?
  4. What is the management of Temporal Arteritis?
  5. What are some early and late complications of Temporal Arteritis?
  6. Discuss the DON’T STOP Mnemonic for STEROIDS
A
  1. A medium-large vessel vasculitis which is associated with Polymyalgia Rheumatica (PMR)
  2. Headache, usually unilateral, in temporal / forehead region. `
    Visual disturbances, secondary to anterior ischaemic optic neuropathy
    Tender, palpable temporal artery
    Jaw claudication, tiredness on talking, chewing
    Low grade fever
    Lethargy
    Night sweats
  3. ESR → Raised, above 50, Temporal artery biopsy → skip lesions and multinucleated giant cells, Duplex US → Hypoechoic halo sign of temporal artery, FBC → Normocytic anaemia with thrombocytosis, ALP → Raised, CRP → May be raised
  4. Steroids: 40-60mg, should see a rapid response within 24-48 hours, Aspirin: 75mg, reduces vision loss and strokes, PPI: GI protection from steroids, Referral to Ophthalmology for same day review, Vascular surgeons for temporal artery biopsy, and Rheumatology for diagnosis
  5. Early → vision loss, CVA, Late → CVA, relapse, steroid related complications, aortitis (aneurysm or dissection)
6. DON'T - don't stop steroids, risk of adrenal crises
S - Sick day rules
T - Treatment card
O - Osteoporosis prevention
P - PPI
27
Q

MIGRAINE

  1. What are the clinical features of a migraine?
  2. What are common triggers to a migraine?
  3. What are the five stages of a migraine? How long do they last?
  4. What is the first-line management of an acute migraine attack?
  5. What is the first-line management of an acute migraine attack in children?
  6. What is the second-line management of an acute migraine attack?
  7. How is an acute migraine attack managed if precipitated by menstruation?
  8. How is an acute migraine attack managed during pregnancy?
  9. When would you offer prophylaxis for patients with migraine?
  10. What first-line medication would you give as prophylaxis for migraine?
  11. What can be used as “mini-prophylaxis” of migraines caused by menstruation?
  12. What first-line medication would you give as migraine prophylaxis in a women of childbearing age and why?
  13. What is second-line for migraine prophylaxis?
  14. What supplement may reduce the frequency and intensity of migraines?
  15. Is HRT safe in women with migraines?
  16. What is an acephalic migraine?
  17. What is Status Migrainosus?
  18. What is a Chronic Migraine?
  19. What is a Hemiplegic Migraine?
A
  1. What are the clinical features of a migraine?
    • Severe, unilateral, throbbing headache
    • Associated nausea, photophobia, phonophobia
    • May have nausea and vomiting
    • May want to retreat into a dark, quiet room
    • Attacks can last up to 72 hours
    • May have an aura → visual, progressive, lasts 5-60 minutes with transient hemianopic disturbance
  2. What are common triggers to a migraine?
    • Stress
    • Dehydration
    • Foods → chocolate, cheese, caffiene
    • Bright lights
    • Strong smells
    • Menstruation
    • COCP
  3. What are the five stages of a migraine? How long do they last?
    • Premonitory / prodrome → 3 days prior
    • Aura → up to 60 mins
    • Migraine → from 4 - 72 hours
    • Resolution stage
    • Post-dromal / recovery phase
  4. Oral triptan + NSAID or… Oral triptan + Paracetamol
  5. As above, however change Oral Triptan → Nasal Triptan
  6. Non-oral metoclopramide or Prochlorperazine. Consider a non oral NSAID or Triptan
  7. Mefanamic acid OR Aspirin + Paracetamol + Caffeine
  8. Paracetamol is first line. NSAIDs is second line during 1st and 2nd trimester
  9. If they have 2 or more migraine attacks per month
  10. Topiramate or Propanolol
  11. Fovatriptan or Zolmitriptan
  12. Propranolol, because Topiramate is teratogenic and can reduce contraceptive efficacy
  13. 10 acupuncture sessions over 5-8 weeks
  14. Riboflavin, 400mg OD
  15. Yes - however may make migraines worse
  16. Migraine aura without a headache
  17. A headache lasting longer than 3 days / 72 hours
  18. Migraine attacks >15 days a month for 3 months
  19. Migraine with hemiplegia
28
Q

CAUDA EQUINA SYNDROME

  1. What is Cauda Equina Syndrome?
  2. How many vertebrae is the spinal column comprised of?
  3. How many spinal nerve pairs are there?
  4. What is the function of the nerves in the Cauda Equina?
  5. What are the symptoms of Cauda Equina Syndrome?
  6. What are some causes of Cauda Equina?
  7. What is the first-line investigation of Cauda Equina Syndrome?
  8. What is the management of Cauda Equina Syndrome?
A
  1. A rare syndrome caused by direct compression to the cauda equina
  2. 33 vertebrae in total → 7 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral and 4 Coccygeal
  3. 31 spinal nerve pairs in total → 8 Cervical, 12 Thoracic, 5 Lumbar, 5 Sacral, 1 Coccygeal
  4. Motor innervation to → Genitalia, Internal + External Sphincter, Detrusor muscle, Leg Muscles. Sensory innervation to → Leg
  5. Reduced bowel and bladder control, Reduced sexual function, Saddle anaesthesia, Lower sciatic back pain, Loss of anal tone
  6. Most commonly caused by lumbar disc herniation, spinal stenosis, Ankylosing spondylitis, Spondylolisthesis, Trauma
  7. Urgent MRI spine within 6 hours
  8. Treat the underlying cause of Cauda Equina Syndrome

Surgical decompression → If due to disc herniation, trauma, tumours, abscess (if symptoms appear suddenly)

Antibiotics → If due to abscess

Anti-inflammatories / corticosteroids → If due to degenerative disease (if symptoms appear gradually)

Lie the patient down flat

29
Q

SPONTANEOUS INTRACRANIAL HYPOTENSION

  1. What is it?
  2. Risk factors?
  3. Features?
A
  1. Rare cause of headache caused by a CSF leak
  2. Connective tissue disorders i.e. Marfan’s
  3. Strong postural relationship with headache, worse when upright. Patients may be bedbound
30
Q

CATAPLEXY and NARCOLEPSY

  1. What is Cataplexy and its features?
  2. What is Cataplexy associated with?
  3. What are the features of Narcolepsy?
  4. Onset of Narcolepsy?
A
  1. Sudden and transient loss of muscular tone, caused by strong emotion i.e. laughter, being frightened. Lead to collapse
  2. Narcolepsy
  3. A condition of hypersomnolence, sleep paralysis, vivid hallucinations, cataplexy
  4. Teenage years
31
Q

REFLEXES

  1. The ankle jerk reflex is controlled by?
  2. The knee reflex is controlled by?
  3. The biceps reflex is controlled by?
  4. The triceps reflex is controlled by?
A
  1. S1-S2
  2. L3-L4
  3. C5-C6
  4. C6-C7
32
Q

BRACHIAL PLEXUS ANATOMY

  1. What is the motor supply of the Median Nerve?
  2. What is the sensory supply of the Median Nerve?
  3. Injury of Median Nerve causes what?
  4. What is the motor supply of the Ulnar Nerve?
  5. What is the sensory supply of the Ulnar Nerve?
  6. Injury of Ulnar Nerve is seen in what fracture?
  7. What is the motor supply of the Radial Nerve?
  8. What is the sensory supply of the Radial Nerve?
  9. Injury of Radial nerve is seen in what fracture?
A
  1. LOAF: Lateral 2 lumbricals, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis
  2. Palmar aspect of lateral 3.5 fingers
  3. Carpal Tunnel Syndrome
  4. All hand muscles except LOAF
  5. Palmar aspect of medial 1.5 fingers
  6. Medial epicondyle fracture “claw hand”
  7. Extension of forearm, wrist, fingers, thumb
  8. Dorsal aspect of 1st and 2nd metacarpals
  9. Humeral midshaft fracture “wrist drop”
33
Q

HEADACHE RED FLAGS

  1. What are some headache red flags?
A
  • Compromised immunity, i.e. HIV / immunosuppression
  • Age below 20, history of cancer
  • History of cancer with known mets to brain
  • Vomiting with no obvious cause
  • Worsening headache with fever
  • Sudden onset “thunderclap” headache reaching intensity <5mins
  • New neurological deficit
  • New onset cognitive dysfunction
  • Change in personality
  • Impaired consciousness level
  • Recent head trauma
  • Headache triggered by cough, sneeze, exercise - ?ICP
  • Orthostatic headache
  • Symptoms of GCA / acute narrow angle closure glaucoma
  • Change in characteristics of headache
34
Q

TENSION TYPE HEADACHE

  1. What are the clinical features of TTH?
  2. What may be some triggers for TTH?
  3. What is a Chronic TTH?
  4. What is the acute management of TTH?
  5. What is the prophylaxis of TTH?
A
  1. Bilateral, tight-banded headache, of lower intensity than a migraine. Typically no nausea, vomiting, or visual changes
  2. Stress, depression, alcohol, skipping meals, dehydration
  3. > 15 or more days
  4. Aspirin, paracetamol, NSAIDs
  5. 10 sessions of acupuncture or low dose amitriptyline
35
Q

SINUSITIS HEADACHE

  1. What is it?
  2. What are the features?
  3. What is the management?
  4. What is the prognosis?
A
  1. A headache caused by inflammation of the ethmoid, maxillary, frontal and sphenoid sinuses
  2. Facial pain behind nose, forehead, eyes. Tenderness of sinuses
  3. Nasal irrigation, sometimes ABX may be used or steroids
  4. Improves within 2-3 weeks
36
Q

CLUSTER HEADACHE

  1. What is it?
  2. What are the features?
  3. What are the triggers?
  4. What patients is it more common in?
  5. What is the acute management?
  6. What is the prophylaxis of cluster headache?
A
  1. Severe headaches which occur in several clusters for days / weeks, followed by a pain free period lasting 1-2 years
  2. Severe, unilateral headache, stabbing in character behind the eye. Redness, tearing eye, small pupil (MOISIS), eyelid drooping (ptosis), nasal discharge, sweating
  3. Alcohol, strong smells, exercise
  4. Common in men, smokers, aged 30-50 years old
  5. OXYGEN HIGH FLOW, SUBCUTANEOUS TRIPTANS
  6. VERAPAMIL
37
Q

POST-LUMBAR PUNCTURE HEADACHE

  1. How common is it?
  2. Which patients are particularly at risk?
  3. When does it develop after LP? How long does it last?
  4. What are the clinical features?
  5. What is the management?
A
  1. Occurs in 1/3 of patients with LP, due to CSF leak
  2. Seen in women, especially those with low BMI
  3. Typically 1-2 days after LP, however can be upto a week later. Lasts for several days
  4. Worsens when upright, improves on lying down
  5. Supportive management, i.e. rest. Analgesia. If >72 hours, then consider blood patch, saline, caffeine
38
Q

MEDICATION OVERUSE HEADACHE

  1. What are the features?
  2. What medications may cause it particularly?
  3. What is the management?
A
  1. Typically >15 days / month, following after taking regular medications
  2. Opioids and triptans
  3. For simple analgesia / triptans = abrupt withdrawal
    For opioids = gradual withdrawal
39
Q

CERVICAL SPONDYLOSIS HEADACHE

  1. What is it?
A
  1. Osteoarthritis changes in the cervical spine, causing referred headache pain
40
Q

STATUS EPILEPTICUS

  1. What is it defined as?
  2. How is it managed pre-hospital first-line?
  3. How is it managed in hospital first-line?
  4. What is second-line?
  5. What is third-line?
A
  1. Defined as a single seizure lasting >5 minutes, or
    >= 2 seizures within a 5-minute period without the person returning to normal between them
  2. Rectal Diazepam
  3. IV Lorazepam 4mg, repeated after 10-20mins
  4. Phenytoin / Phenobarbital infusion
  5. Induction of general anaesthesia
41
Q

AUTONOMIC DYSREFLEXIA

  1. What is it?
  2. What are the features?
  3. Management?
A
  1. A clinical syndrome caused by spinal cord injury at or above T6, can also be triggered by faecal impaction or urinary retention
  2. Severe hypertension, bradycardia, flushing, sweating above the level of the lesion
  3. Treat underlying cause, remove the stimulus and manage the life-threatening HTN and bradycardia
42
Q

MYASTHENIA GRAVIS

  1. What is Myasthenia Gravis?
  2. What is the epidemiology of Myasthenia Gravis?
  3. What is the pathophysiology of Myasthenia Gravis?
  4. What are some associations of Myasthenia Gravis?
  5. What are some key features of Myasthenia Gravis?
  6. How can Myasthenia Gravis be diagnosed?
  7. What is the management of Myasthenia Gravis?
  8. What is a Myasthenic Crisis?
  9. What is the management of a Myasthenic Crisis?
A
  1. An autoimmune disorder resulting in weakness, caused by insufficient functioning AChR
  2. Commonly affects females around age 40, males around 60
  3. In 85% of cases → antibodies against AChR, preventing ACh from binding, in 15% of cases → antibodies against MuSK or LRP4
  4. Thymoma (15% of cases), Thymic hyperplasia, Autoimmune disorders → Pernicious anaemia, autoimmune thyroid disease, rheumatoid arthritis, SLE
  5. Muscle fatigability → during repetitive movements and activity, improves with rest, Extraocular muscle weakness → diplopia, Proximal muscle weakness → face, neck, limb, girdle, Ptosis, Dysphagia
  6. AChR antibodies, MuSK antibodies, LRP4 antibodies, CT / MRI of thymus, Edrophonium / Tensilon test → IV Edrophonium / Neostigmine will briefly and temporarily relieve the weakness, Single fibre electromyography, Creatinine kinase → normal
  7. LONG ACTING ACETYLCHOLINESTERASE INHIBITORS → Pyridostigmine first line, immunosupression, Thymectomy
  8. Life-threatening complication of Myasthenia Gravis, Often triggered by Respiratory Tract Infection, Can cause respiratory failure due to weakness in muscles of respiration
  9. May need NIV + BiPaP, May need intubation and ventilation
43
Q

CHARCOT-MARIE-TOOTH DISEASE

  1. What is it?
  2. What is the inheritance pattern?
  3. Is it mainly sensory, motor, or both?
  4. What are the clinical features?
  5. What is the management?
  6. What is another neurological condition which causes predominantly motor loss?
A
  1. The most common cause of inherited peripheral neuropathy
  2. Autosomal dominant
  3. Features of sensory and motor loss, but predominantly motor loss
  4. Champagne bottle legs due to distal muscle wasting, reduced tendon reflexes, high arched foot, loss of ankle dorsiflexion / foot drop, hand weakness, reduced tone
  5. No cure, mainly occupational / physical therapy
  6. Guillin-Barre syndrome
44
Q

LAMBERT EATON SYNDROME

  1. What is it?
  2. What are the features of Lambert Syndrome?
  3. Compare and contrast how it is different to Myasthenia Gravis on investigation?
  4. Compare and contrast how it is different to Myasthenia Gravis in terms of features?
  5. What are some investigations you may want to do?
  6. What is the management?
A
  1. A myasthenic syndrome seen in association with small cell lung cancer and also breast / ovarian cancer
  2. Limb girdle weakness affecting the lower limbs first, hyporeflexia. Autonomic features i.e. dry mouth, impotence, difficulty urinating
  3. Repeated muscle contractions will increase muscle strength, whereas in Myasthenia Gravis it will decrease
  4. No ophthalmoplegia / ptosis
  5. EMG (increased response on stimulation) Investigation for SCLC / breast / ovarian cancer
  6. Treat the underlying malignancy if there is one, and Steroids / Azathioprine, and Amifampridine (in BNF), and IVIG
45
Q

GUILLAIN-BARRE SYNDROME

  1. What is it?
  2. What are the features?
  3. What is an important thing to ask about in the history?
  4. What is GBS usually caused by?
  5. What is the clinical course?
  6. What are some investigations?
  7. What is the management?
A
  1. An acute paralytic polyneuropathy, affecting the peripheral neurones
  2. Symmetrical ascending weakness (from lower legs to up body), reduced reflexes. Motor > sensory however may have some sensory loss. May have leg / back pain. They may have diplopia, respiratory muscle weakness
  3. Any previous history of gastroenteritis?
  4. Campylobacter jejuni, EBV, CMV
  5. Usually 4 weeks from infection, peaks within 2-4 weeks, recovery for months - years
  6. Nerve conduction studies, LP for CSF will show HIGH PROTEIN
  7. IVIG, plasma exchange, supportive care, VTE prophylaxis
46
Q

NEUROFIBROMATOSIS

  1. What is it?
  2. What are the features?
  3. What is the inheritance pattern?
  4. What is needed for diagnosis?
  5. What investigations could you also do?
  6. What is the management?
A
  1. A genetic condition that causes nerve tumours (neuromas), to develop throughout the nervous system and can cause neurological and structural problems
2. 
C - Cafe-au-lait spots (darker than skin)
R - Relative with NF1
A - Axillary / inguinal freckles
BB - Bony dysplasia
I - Iris Hamartomas
N - Neurofibromas
G - Glioma of the optic nerve
  1. Autosomal dominant
  2. 2 of the 7 points above
  3. Genetic testing for relatives, X-Rays for bone pain / bony lesions, CT / MRI to investigate for brain / spinal cord lesions
  4. Supportive management
47
Q

TUBEROUS SCLEROSIS

  1. What is it?
  2. What are the features?
  3. What is the inheritance pattern?
A
  1. A genetic, multi-system disorder condition; characterically causing hamartomas which are benign, neoplastic growths of tissue
  2. ASASAP
A - Ashleaf spots
S - Shagreen patches
A - Angiofibromas
S - Subungal fibromata
A - Au lait spots (cafe)
P - Poliosis (white hair)
  1. Autosomal dominant
48
Q

TRANSIENT ISCHAEMIC ATTACK

  1. What is a Transient Ischaemic Attack?
  2. What is a crescendo TIA? Why is this a red flag?
  3. What are the features?
  4. What are some investigations for TIA?
  5. What is the management of a TIA?
  6. Why shouldn’t statins be given immediately in a patient with a TIA / stroke, but 48 hours later?
A
  1. A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without infarction
  2. When you have >2 episodes of TIAs in a week, may precede a stroke
  3. Sudden onset of limb weakness, facial weakness, speech disturbances, visual or sensory loss which has since improved
  4. Diffusion weighted MRI to determine cardiac territories involved, and carotid Ultrasound to determine if stenosed

5.

  • Seen by stroke specialist within 24 hours
  • If had crescendo TIA, admit + observe in hospital
  • NO Driving until seen by the specialist

Medical management:

  1. Immediate antithrombotic therapy, 300mg Aspirin
  2. Secondary prevention of a Stroke / TIA:
    - Clopidogrel
    - Atorvastatin, 80mg (not immediately)
    - Manage HTN and Diabetes well

Surgical management:
1. Carotid endarterectomy if >70% stenosis

  1. Risk of haemorrhagic transformation
49
Q

STROKE

  1. What is it?
  2. What are the two main types of stroke? Define them
  3. What are examples of Ischaemic strokes?
  4. What are examples of Haemorrhagic stroke?
  5. What are the general features of a stroke?
  6. What are the typical features of a brainstem stroke?
  7. What are the typical features of a lacunar stroke?
  8. What is the Oxford Bamford Classification used for?
  9. What is a TACI? How is it defined on Oxford Bamford classification?
  10. What is a PACI? How is it defined on Oxford Bamford classification?
  11. What is a POCI?
  12. What screening tools can be used in investigating suspected stroke patients?
  13. What are some investigations for a patient with suspected stroke?
  14. What is the initial management of a stroke?
  15. Why shouldn’t BP be controlled in acute setting for stroke?
  16. Why shouldn’t statins be given in immediate setting for stroke?
  17. What is the later management of a stroke patient?
  18. What are some contraindications to thrombolysis?
A
  1. A sudden interruption in the vascular supply of the brain
  2. Ischaemic stroke which is a blockage in vessel, occluding blood flow. Secondly, haemorrhagic stroke is where blood vessels “bursts” leading to a reduction of blood flow
  3. Thrombotic stroke and Embolic stroke
  4. Intracerebral haemorrhage (within brain) and those outside of brain i.e. subarachnoid
  5. Motor weakness, speech weakness, swallowing issues, visual fields defects, balance issues
  6. Locked in syndrome or quadriplegia
  7. Pure motor, pure sensory, mixed motor + sensory, or ataxia
  8. A classification system for Ischaemic stroke
  9. Total anterior circulation infarct (Middle + anterior cerebral arteries), must have 3/3 of:
    3 points:
  10. Unilateral hemiparesis and/or hemisensory loss
  11. Homonymous hemianopia
  12. Higher cognitive dysfunction i.e. dysphasia
  13. Partial anterior circulation infact (part of anteior circulation artery affected), must have 2/3 of:
    3 points:
  14. Unilateral hemiparesis and/or hemisensory loss
  15. Homonymous hemianopia
  16. Higher cognitive dysfunction i.e. dysphasia
  17. Posterior circulation infarct (affects vertebrobasilar arteries), with one of following:
  18. Cerebellar / brainstem syndromes
  19. Loss of consciousness
  20. Isolated homonymous hemianopia
  21. ROSIER (Risk of stroke in emergency room)
  22. Bedside: Observations, glucose
    Bloods: FBC, U&Es, Lipid profile, serum glucose, coagulation screen, INR if on Warfarin
    Imaging: 12-lead ECG, CT Head w/o contrast (rule out haemorrhagic stroke), Diffusion weighted MRI
    Special tests: Carotid Ultrasound
    • Perform ABCDE assessment, elicit risk via ROSIER
    • Exclude hypoglycaemia (mimic stroke)
    • Refer to specialist stroke unit
    • Immediate brain CT to exclude haemorrhagic stroke
    • Aspirin 300mg STAT for 2 weeks after ruling out
    • If presented before 4.5 hours, perform thrombolysis via Alteplase
    • Give secondary prevention i.e. Atorvastatin 80mg after 48 hours and Clopidogrel 75mg
      Surgical:
    • Carotid endarectomy to reduce carotid stenosis
    • Thrombectomy
  24. Because lowering BP will reduce perfusion to brain
  25. Because statins may cause hemorrhagic transformation
17. 
Maintain BP and diabetes control in an outpatient setting
Stroke rehabilitation
- Nurses
- Speech and language (SALT)
- Nutrition and dietetics
- Physiotherapy
- Occupational therapy
- Social services
- Optometry and ophthalmology
- Psychology
- Orthotics
  1. Previous Intracranial bleed, active bleeding, space occupying lesion, GI bleed recently, pregnancy, uncontrolled HTN, esophageal varices
50
Q

STROKE BY ANATOMY

  1. What would an anterior cerebral artery infarct produce?
  2. What would a middle cerebral artery infarct produce?
  3. What would a posterior cerebral artery infarct produce?
  4. What does a Weber’s syndrome infarct produce?
  5. What is lateral medullary syndrome caused by?
  6. What are the features of Lateral Medullary Syndrome?
  7. What are features of a Retinal Ophthalmic Artery infarct?
  8. What are the features of a Basilar artery infarct?
A
  1. Contralateral hemiparesis and sensory loss, Lower limbs affected more than upper limbs
  2. Contralateral hemiparesis and sensory loss, Upper limbs affected more than lower limbs. Contralateral homonymous hemianopia and aphasia
  3. Contralateral homonymous hemianopia WITH MACULAR SPARING. Visual agnosia
  4. Ipsilateral CN3 palsy, with contralateral weakness of upper and lower body
  5. Posterior, inferior cerebellar artery
  6. Cerebellar features: ataxia, nystagmus
    Brainstem features:
    - Ipsilateral dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
    - Contralateral: limb sensory loss
  7. Amaurosis fugax
  8. Locked in syndrome

medicine, year 4, elderly, neuro, msk (3 decks)

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