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Phase 3 > Week 12 > Flashcards

Week 12 Flashcards

1
Q

What is horner’s syndrome?

A

Results from ipsilateral disruption of cervical/thoracic sympathetic chain

Consists of:

  • miosis
  • ptosis
  • apparent enopthalmos
  • anhidrosis
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2
Q

What is the clinical presentation of radial neuropathy?

A

Most common cause: entrapment at spiral groove

Presenting symptoms:

  • wrist and finger drop (wrist and finger extension weakness)
  • usually painless

Sensory change over prone surface of thumb and lateral side of the hand as well as lower half of finger 2 and lateral half of finger 3

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3
Q

What is the clinical presentation of ulnar neuropathy?

A

Most common cause: entrapment at ulnar groove (medial epicondyle of humerus)

Presenting symptoms:

  • may be history of trauma at elbow
  • sensory disturbance and weak grip
  • usually painless

Sensory change over medial aspect of the hand; half of finger 3,4 and 5

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4
Q

What is the clinical presentation of medial neuropathy?

A

Most common cause: entrapment within carpal tunnel at wrist

Presenting symptoms:

  • history of intermittent nocturnal pain, numbness and tingling, often relieved by shaking hand
  • patient may complain of weak grip
  • +ve Tinel’s sign/Phalen’s test

Sensory change over finger tips of thumb, 2,3 and 4 and supine surface of hand from half of finger 4 to thumb

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5
Q

What is the clinical presentation of common peroneal neuropathy?

A

Most common cause: entrapment at fibular head

Presenting symptoms:

  • may be history of trauma, surgery or external compression
  • acute onset foot drop + sensory disturbance
  • usually painless

Motor weakness:

  • Tibialis anterior resulting in ankle dorsiflexion weakness
  • Extensor hallicus longus resulting in great toe extension weakness
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6
Q

What is the clinical presentation of femoral neuropathy?

A

Most common cause: haemorrhage/trauma

Presenting symptoms:

  • weakness of quadriceps
  • weakness of hip flexion
  • numbness in medial shin

Sensory change over medial aspect of lower leg

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7
Q

What are the causes of length dependent axonal neuropathy?

A 
Diabetes
Alcohol
Nutritional deficiency (folate/B12)
Immune mediated (RA, SLE, vasculitis)
Metabolic/endocrine (renal failure, hypothyroidism)
Infectious (HIV, Hep B&C)
Genetic
Neoplastic (myeloma)
Paraneoplastic
Critical illness

Drugs: isoniazid, cisplatin, amiodarone, gold

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8
Q

Describe the clinical presentation of neuropathy:

A

Depends on the type and distribution of affected fibres

Motor: weakness/muscle atrophy

Sensory:
large (myelinated) fibres -> sensory ataxia, loss of vibration sense +/- tingling
small (thin/unmeylinated fibres) -> impaired pin prick, temperature, painful, burning, numbness and tingling

Autonomic:
-> postural hypotension, erectile dysfunction, GI disturbance, abnormal sweating

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9
Q

Describe Gullain-Barre syndrome:

A
  • Acute inflammatory demyelinating neuropathy
  • Post-infectious autoimmune aetiology (e.g. campylobacter, CMV, EBV)
  • Progressive (ascending) weakness over days
  • Flaccid, quadraparesis with areflexia
  • +/- respiratory/bulbar/autonomic involvement
  • treated with IVIG or apheresis
  • CIDP: chronic form (steroid and IVIG responsive)
  • Demyelinating pattern on nerve conduction is supportive in diagnosis of GB, as well as high protein levels in CSF
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10
Q

Describe myasthenia gravis:

A

Pathogenesis and investigation:

  • Autoimmune disorder; antibodies to acetycholine receptor at post-synaptic NMJ
  • May be associated with thymic hyperplasia or thymoma (residual tumour of thymus gland)
  • Affects young women in 20s and older men in 70s
  • Fatiguable weakness of ocular. bulbar, neck, respiratory and/or limb muscles

Investigation and management

  • Antibodies to AChR present in 85% of cases
  • Single fibre EMG and repetitive nerve stimulation also abnormal
  • Managed with pyridostigmine (anti-acetylcholineesterase) and immunosuppressive therapies (steroids and IVIG)
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11
Q

What is the difference between primary and secondary headache?

A

Primary headache = headache and its associated is the disorder (eg migraine, tension-type headache, clutster headache)

Secondary headache = secondary to underlying cause (eg subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis, high/low intracranial pressure, drug-induced)

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12
Q

What are the important features in headache history?

A
  • Onset
    • time to maximal symptoms
    • circumstances at onset
  • Severity and quality of pain
    • pain scale 1-10
    • throbbing/pulsatile/’vice-like’/stabbing)
  • Location/radiation of pain
  • Presence of aura/prodrome
  • Periodicity
    • duration and frequency
  • Associated features
  • Age at onset of headache
  • Triggers/exacerbating/relieving factors
  • Family history
  • Social/employment history
  • Medication history
  • Co-morbid depression/sleep disturbance
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13
Q

What clinical signs are important when examining a patient with headache?

A

General/systemic:
Reduced conscious level, BP/pulse, pyrexia, meningism, skin rash, temporal artery tenderness

Cranial nerve:
Pupillary responses. visual fields +/- blind spot, eye movements, fundoscopy

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14
Q

What are red flags in pt with headache?

A
  • Age >50 years
  • Thunderclap headache
  • Focal/non-focal neurological deficit
  • Worsening of symptoms with posture (high/low CSF pressure headache), valsalva (coughing/straining), or physical exertion
  • Early morning headaches
  • Systemic symptoms: fever, weight loss
  • Seizures, meningism
  • Termporal artery tenderness/jaw claudication
  • Specific situations- cancer, pregnancy, post-partum, HIV/immunosuppression

SNOOPT
Systemic symptoms, neurological signs or symptoms, older age at onset, onset is acute (under 5 minutes), previous headache history is different/absent, triggered headache (valsalva or posture)

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15
Q

Describe migraine:

A
  • Female preponderance
  • Prevalence highest in 25-55yr
  • Positive FHx
  • Triggers; hormonal, weather, stress, hunger, sleep disturbance, exertion, alcohol, foods
  • Can be with (30%) or without aura

Management:

  • lifestyle: avoid triggers, reduce caffeine/alcohol intake, encourage regular meals and sleep patterns
  • acute management: simple analgesia (paracetamol, aspirin, NSAIDs), triptans (sumatriptan), +/- antiemetic
  • prophylaxis: beta-blockers, tricyclic antidepressants, anti-epilepsy drugs
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16
Q

Describe features of high and low pressure headaches:

A

High:

  • optic disc swelling (papilloedema)
  • enlarged blind spot
  • impaired visual acuity/colour vision
  • 3 and 6 nerve palsy

Low:

  • worse on sitting/standing up and relieved by lying down
  • results from CSF leakage
  • causes: post-lumbar puncture, spontaneous intracranial hypotension)
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17
Q

Describe assessment and investigation of thunderclap headache:

A

Causes: subarachnoid haemorrhage, intracerebral haemorrhage, arterial dissection

Investigations: primary aim is to identify SAH

  • bloods
  • 12-lead ECG
  • urgent CT brains
  • lumbar puncture
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18
Q

Describe the epidemiology of stroke:

A

Modifiable RFs

  • BP
  • Smoking
  • DM
  • Heart disease (valvular, ischaemic, AF)
  • PVD
  • past TIA
  • Increased PCV
  • Carotid bruit
  • The pill
  • Hyperlipidaemia
  • Alcohol use
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19
Q

Describe the pathological processes that can result in stroke:

A

Haemorrhagic: rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma

Intracranical bleed causes:

  • small vessel disease (deep perforating vasculopathy)
  • amyloid angiopathy
  • abnormalities in blood vessels
  • blood clotting deficiencies
  • haemorrhagic transformation of an infarct
  • tumours
  • drug useage: cocaine, amphetamine

Ischaemic: an episode of neurological dysfunction caused by focal cerebral, spinal or retinal infarction

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20
Q

Describe the clinical presentation of stroke:

A

TACS: total anterior circulation syndrome

  • hemiparesis + higher cortical dysfunction + hemianopia
  • usually proximal MCA or ICA occlusion

PACS: partial anterior circulation syndrome

  • isolated higher cortical dysfunction OR
  • any 2 of hemiparesis, higher cortical dysfunction, hemianopia
  • usually branch MCA occlusion

POCS: posterior circulation syndrome

  • isolated hemianopia OR
  • brainstem syndrome
  • can include perforating arteries, PCA or cerebellar arteries

LACS: lacunar syndrome

  • pure motor stroke
  • OR pure sensory stroke
  • OR sensorimotor stroke
  • OR ataxic hemiparesis
  • OR clumsy hand-dysarthria
  • perforating artery/small vessel disease
21
Q

Describe the management of stroke:

A

3 treatments proven to be effective:

  • thrombolysis
    • within 4.5 hrs of symptom onset
  • thombectomy
    • within 6-8hrs of symptom onset
  • admission to a stroke unit
    • coordinated care
    • short-long term therapy
    • prevent aspiration

The earlier treatment is given the better

Brain imaging is important for diagnosis and management of an acute stroke

22
Q

Describe the pathogenesis and clinical presentation of SAH:

A

Aneurysm formation; localised dilatation of artery

RFs: smoking, female sex, hypertension, +ve FHx, ADPCK, Ehlers Danlos, coarctation of the aorta

Exam looking for:

  • photophobia
  • meningism
  • subhyaloid haemorrhages
  • vitreous haemorrhages
  • speech and limb disturbances
  • pulmonary oedema

History:

  • sudden onset headache
  • LOC, seizures, visual, speech and limb disturbances
  • sentinel headache
23
Q

Describe the investigation and management of SAH:

A

CT:

  • confirms diagnosis
  • clues to aetiology
  • identifies complications
  • prognostic: fisher grade

Other investigations:

  • LP (xanthochromia)
  • CTA/MRA
  • Digital subtraction angiogram

Management:

  • surgical clipping
  • endovascular (coils, stents and glue)
  • conservative
24
Q

What are the complication of SAH?

A
  • Re-haemorrhage
  • Delayed ischaemia
  • Hydrocephalus
  • Hyponatraemia
  • ECG changes (CVS symptoms due to output of catecholamines)
  • LRTI, PE, UTI
  • Seizures
  • Might also require sequential DVT prophylaxis
25
Q

Outline GCS:

A

Eye opening:

  1. Spontaneously
  2. To speech
  3. To pain
  4. No response

Verbal response:

  1. Oriented to time, person and place
  2. Confused
  3. Inappropriate words
  4. Incomprehensible sounds
  5. No response

Motor response

  1. Obeys command
  2. Moves to localised pain
  3. Flex to withdraw from pain
  4. Abnormal flexion
  5. Abnormal extension
  6. No response
26
Q

Describe prevalence of MS in Scotland:

A

Scotland has highest incidence and prevalence in world
Approx 1 in 600 people in Scotland have MS
Highest prevalence in Orkney

27
Q

Describe pathology of MS:

A

Acute episodes of inflammation are associated with focal neurological deficits

Demyelinating results in loss of neurological function:

  • weak leg
  • visual loss
  • urinary incontinence

Optic neuritis, clinically isolated syndromes, transverse myelitis and radiologically isolated syndromes may all develop into MS

28
Q

Describe presentation and diagnosis of MS:

A

MS is diagnosed where there is evidence of 2 or more episodes of demyelination disseminated in space and time

Usually presents:

  • neuro symptoms that develop over a few days
  • history of transient neuro symptoms that have lasted for more than 24 hours and spontaneously resolved
  • ‘hidden’ relapses should always cause suspiscion of MS
    • optic neuritis/visual disruption
    • Bell’s palsy
    • labyrinthitis
    • sensory sypmtoms
    • bladder symptoms in young man/woman without children

SEE SUMMARIES FOR SYMPTOM DIAGRAM

29
Q

Outline role of MRI, LP and VERS in MS diagnosis:

A

MRI:

  • image brain and cervical spine with gadolinium contrast
  • possible to make diagnosis of MS with one scan:
    • evidence of dymyelination in 2 regions can indicate dissemination in space
    • if enhancing and non-enhancing areas of dymyelination are seen this can indicate dissemination in time

LP: look for presence of oligoclonal bands (need matched blood sample)

VERS:

  • measure conduction of nerve signals in optic nerve to look fir subclinical optic neuritis
  • conduction will be slower if a patient has had optic neuritis in the past
30
Q

Describe treatment for MS:

A

Relapse:
- steroid regime

RRMS: DMARDs

  • alemtuzumab
  • natalizumab
31
Q

Describe treatment for MS:

A

Relapse:
- steroid regime (+ PPI for gastric protection)

RRMS: DMARDs
- alemtuzumab
- natalizumab
oral treatments
- fingolimod
- dimethyl fumarate
32
Q

Describe the pathological changes seen in Parkinson’s disease:

A
  • Basal ganglia have role in maintaining posture and initiating voluntary movement
  • Loss of dopaminergic neurones within substantia nigra
  • Surviving neurones contain Lewy bodies
  • PD manifests clinically after loss of approximately 50% of dopaminergic neurones
33
Q

Describe the CFs of PD:

A

Bradykinesia: slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
Also with muscular rigidity, 4-6 Hz rest tremor (pill-rolling), posutral instability

Non-motor symptoms:

  • neuropsychiatric;
    • dementia, depression, anxiety
  • autonomic;
    • constipation, urinary urgency/nocturia, erectile dysfunction, excessive salivation/sweating, postural hypotension
  • sleep;
    • REM sleep behaviour disorder, restless leg syndrome, daytime somnolence
  • other;
    • reduced olfactory function, fatigue, pain and sensory symptoms
34
Q

Describe investigations of PD:

A

Bloods:
- if tremor present: TFTs, copper/caeruloplasmin
Structural imaging:
- CT/MRI brain normal in PD
- Abnormal in vascular parkinsonism, Parkinson plus disorders
Functional imaging:
- Imaging of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative parkinsonism

35
Q

Outline the principles of drug management of PD:

A

Pharmacological aim: restore dopamine levels
Clinical aim: improve motor symptoms / improve QOL

Drug classes:
• L-dopa
• Dopamine agonists
• MAO-B inhibitors
• COMT- inhibitors

L-dopa:
- taken up by dopaminergic neurones and decarboxylated to dopamine within presynaptic terminals
- prescribed with dopa-decarboxylase inhibitor
Longer term: Approx. 50% of patients develop motor complications after 5 years L-dopa
– Fluctuation in motor response
– Dyskinesia – most commonly
chorieform movements at peak dose

36
Q

Describe the role of MDT in PD:

A 
Multi-disciplinary team
• GP
• Neurologist / care of the elderly physician
• Parkinson’s disease nurse specialist
• Physiotherapist
• Speech and language therapist
• Psychiatrist
• Psychologist
• Occupational therapist
• (Palliative care team)
• (Neurosurgeon)
37
Q

What is in differential diagnosis of PD?

A
  • Diagnosis of PD is largely clinical diagnosis
  • Diagnostic certainty improves with follow-up
  • Disorders commonly mistaken for PD;
    • benign tremor disorders (e.g. essential tremor)
    • dementia with Lewy bodies
    • vascular parkinsonism
    • Parkinson plus disorders (e.g. progressive supranuclear palsy, multiple system atrophy)
    • Drug-induced parkinsonism/tremor
38
Q

Outline causes for LOC:

A
  • Syncope
  • Migraine
  • Narcolepsy/cataplexy
  • Transient global amnesia
  • Panic attacks
39
Q

Define seizures and epilepsy:

A

Seizure: episode of neuronal hyperactivity causing signs and symptoms

Seizures can be focal or generalised
Focal: area of abnormality in otherwise normal brain, which can spread and cause generalised seizure

Generalised: thought to be genetic, arise from generalised tendency to repeated discharges and action potentials

  • potentially disorder of metabolism of NTs or ion channels
  • affects whole brain at once

Epilepsy: at least two unprovoked episodes of seizure

40
Q

Briefly outline types of epilepsy:

A

Focal epilepsy:

  • history trauma/birth injury
  • focal aura/sequelae (including gustatory/sensory/motor features)
  • post-attack confusion/drowsiness
  • automatisms
  • noctural events

GGE features:

  • photo-sensitivity
  • age of onset= 8-26
  • alcohol or sleep deprivation
  • myoclonus (especially in AM)
  • lack of aura
  • seizures within 2 hours of awakeneing
  • FHx of IGE
  • EEG abnormal
41
Q

Discuss investigations of LOC;

A

History: from patient and eye witness

Brain imaging; MRI in younger people

EEG;

  • observe activity on EEG with lying at rest, then hyperventilation, with photic stimulation and watch with drowsiness
  • can also do ambulatory/video telemetry EEG

Systemic provocations

42
Q

Outline long term management of epilepsy:

A

Focal Epilepsy
Lamotrigine, Carbamazepine, Levetiracetam

Generalised Epilepsy
Valproate, Levetiracetam, Lamotrigine

43
Q

Describe status epilepticus:

A 
Status Epilepticus
• repetitive or prolonged epileptic seizures
• a medical emergency
• may cause profound systemic / neuronal
damage
• recognised mortality
Definition
>2 seizures without full recovery
of neurologic function between seizures
or
continuous seizure activity >30 mins
44
Q

What are radiological and lab tests for CNS infection:

A 
CT in suspected meningitis:
 - CT to exclude mass lesion / mass effect, gross cerebral oedema
 - Doesn’t exclude raised ICP
- CT before LP if:
  - GCS ≤ 12
  - CNS Signs
  - Papilloedema
  - Immunocompromised 
  - Seizure
ANTIBIOTICS PRE-CT SCAN

LAB TESTS:

  • history and exam
  • blood cultures (blood PCR)
  • throat culture, viral gargle
  • FBC, U&Es, LFTs, CRP
  • LP
    • cell count, gram stain, culture and PCR
    • protein and glucose
    • viral PCR
45
Q

How are CNS infections managed?

A

Possible BM: IV ceftriaxone

Definitive antibiotic therapy for BM:

  • Meningococcal
    • IV ceftriaxone or ben pen
    • 5-7 days
  • Pneumococcal
    • IV ceftriaxone or ben pen
    • 14 days
  • Listeria
    • IV amox
    • 21 days
46
Q

Describe common pathological processes in common dementias:

A

AD: environmental and genetic factors play a role in accumulation of beta-amyloid peptide resulting in progressive neuronal damage, neurofibrillary tangles and loss of neurotransmitter acetylcholine

VD: cumulative effects of many small strokes, thus sudden onset and stepwise deterioration is characteristic

Lewy Body Dementia: typically with fluctiating cognitive impairment, detailed visual hallucinations and later, parkinsonism. Histology is characterised by Lewy Bodies in brainstem and neocortex

Pick’s: frontal and temporal atrophy without AD histology, genes on on chromosome 9 are important

Other causes are alcohol/drug abuse, repeated head trauma, pellagra, Whipple’s disease, Huntington’s, Parkinson’s

47
Q

Describe clinical presentation of common dementias:

A 
Suspect AD in adults with enduring, progressive and global cognitive impairment: visuo-spatial skill (gets lost), memory, verbal abilities and executive function are all affected
Also anosognosia (lack of insight into the problems engendered by the disease)
Later they may be irritability, mood disturbance, behavioural changes, agnosia (may not recognise self in the mirror)

No standard natural history

48
Q

Discuss investigation of common dementia syndromes:

A

FBC, ESR, U&Es, Ca2+. LFT, TFTs, autoantibodies, B12/folate, syphillis serology
CT/MRI (for vascular damage, haemorrhage or structural pathology)
Consider also EEG, CSF, functional imaging (FDG, PET, SPECT)
Metabolic, genetic and HIV tests if indicated

Phase 3 (14 decks)

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