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Year 4/5 Revision > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the difference between focal and generalised seizures?

A
  • Focal - specific neuro deficit within one region (e.g. temporal) with retained/impaired consciousness.
  • Generalised - simultaneous involvement of both hemispheres with LoC.
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2
Q

What is Jacksonian March?

A

A type of focal seizure of abnormal electrical activity in the frontal lobe where clonic movements (contracting and then relaxing) start in one limb and move proximally through the body.

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3
Q

Seizures can be classified by 3 modes - what are they?

A
  1. Seizure typeLocation (focal/generalised) & motor/non-motor onset
  2. Level of awareness aware/impaired awareness
  3. Other features
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4
Q

List the 5 main epilepsy childhood syndromes according to onset:
* 6mo
* 6-10mo
* 1-5yrs
* 6-8yrs
* Teenage

A
  • West syndrome (full body spasms, poor prognosis, 4-8mo)
  • Dravet’s syndrome (prolonged febrile convulsions)
  • Lennox-Gastaut syndrome (similar to West syndrome but presents later)
  • Benign rolandic epilepsy (focal, facial/tongue/speech paraesthesia often in morning, most common)
  • Juvenile myoclonic epilepsy (full myoclonic seizures often following sleep deprivation)
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5
Q

What are the EEG changes expected in West’s, Lennox Gastaut’s and Benign Rolandic Epilepsy?

A

West’s - hypsarrhythmia
L-G - slow spikes
BRE - centrotemporal spikes

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6
Q

Epilepsy
State the investigations you would do/consider

A
  • Bloods - glucose, U&E
  • EEG
  • ECG
  • MRI Brain
  • Other - LP, urine cultures, ?septic screen
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7
Q

Management for seizures
- community
- hospital
Define status epilepticus

A
  • Community: Rectal Diazepam or Buccal Midazolam
    * Hospital: IV Lorazepm (–> repeat after 10 mins if continue) –> IV Phenobarbitone –> I+V.
  • Prolonged seizure for >5 minutes or 2 seizures without regaining consciousness in between.
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8
Q

3 crtiteria for a brain MRI for investigatiing seizures

A
  1. If seizure happened before age of 2
  2. If unresponsive to 1st line anti-epilpetics
  3. Focal seizures
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9
Q

Usually anti-epileptics are started after the second seizure. NAme the 4 criteria for reasons to start after 1st sezirue.

A
  1. Type of seizure:Focal
  2. EEG findings: unequivocal activity
  3. Further seizure is perceived an unacceptable risk
  4. MRI findings: structural abnormality

note after first seizure cannot drive for 6 months (need to inform DVLA)

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10
Q

Anti-epileptic 1st and 2nd lines for
- generalised motor
- focal
- Absence
- myoclonic (type of generalised absence)

A

For male (*Sodium Valproate CI for women at reproductive age)

  • (1) Sodium valproate (2) Lamotrigine/Levetiracetam
  • (1) Lamotrigine/Levetiracetam (2) Carbamazepine
  • (1) Ethosuximide (2) Sodium Valproate/Lamotrigine
  • (1) Sodum valproate (2) Levetiracetam

Generalised –> generalised absence –> generalised absence myoclonic = C –> E –> L. As the seizure type gets more specific the second line drug is later in the alphabet.

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11
Q

Treatement for West Syndrome

A

Prednisolone (reduces spasms) / Vigabatrin (inhibits breakdown of GABA)

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12
Q

MOA of
- Sodium Valproate (pleiotropic)
- Carbamazepine/Lamotrigine/Phenytoin

A
  • Increased activity of GABA and Na+/Ca2+ channel blockers (stabilsing membrane potential)
  • Na2+/Ca2+ channel blockers

Sodium valproate is the boss drug of epilepsy so makes sense to have multiple mechanisms …..and to be for men (not to be sexist)

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13
Q

Which drug is teratogenic & SEs include liver damage, hair loss & tremor

A

Sodium Valproate (avoid in woman of reproductive age)

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14
Q

Which drug is a P450 inducer & can cause SEs of agranulocytosis and aplastic anaemia

defiency in granulocytes (basophils, neutrophils and eosinophils) -severe form of neutropenia

A

Carbamazepine

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15
Q

Phenytoin’s SEs are folate and vitamin D deficiency - what can this lead to?

A

Megaloblastic anaemia and osteomalacia respectively

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16
Q

3 side effects of Lamotrigine

A

Stevens Johnson syndrome (rash –> shedding of skin), DRESS syndrome, leucopenia

drug reaction wth eosinophilia and systemic symptoms - rash but with organ invovement (lymphadenopathy, fever)

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17
Q

Define status epileptics and its immediate treatment.
What are the 2nd, 3rd and 4th line options if this fails?

A

Seizure lasting >5 mins or 2+ seizures in 1hr.
1) A-E; IM Lorazepam
2) IV Lorazepam (repeat after 10 mins)
3) IV Phenytoin
4) Thiopentate sodium (anaesthesia)

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18
Q

How do you treat status epilepticus in the community? (Buccal or rectal)

A

Buccal Midazolam
Rectal Diazepam

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19
Q

Clinical features of a cluster headache
Prophylaxis - 1st line
Treatment

A
  • Severe onset, localised, severe pain
  • repeated episodes (clusters of attacks) –> disappear –> reappear
  • acute episodes approx 0.5-2hrs long, often same time each day over a few weeks
  • red, swollen, watery, miotic eye
  • sweating, nasal discharge

Prophylaxis
- Verapamil
Treatment
- Sumatriptans SC
Oxygen

Differential: SAH, migraine, venous sinus thrombosis, GCA

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20
Q

4 types of migraine

A

With aura
Without aura
Hemiplegic migraine (stroke mimic)
Silent migraine (aura, no headache)

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21
Q

Prophylactic medical treatments for cluster headaches (3) vs migraine (3)?

A

Cluster - Verapamil (CCB), Lithium, Prednisolone
Migraine - Propanolol, Topiramate (teratogenic), Amitryptiline

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22
Q

Medical treatment options for cluster vs migraine (acute & prophylactic options)

A

Cluster - Triptans (S/C); O2
Migraine - Triptan+ NSAID/paracetamol.
Migraine prophylaxis - Topiramate or Propanolol.

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23
Q

Class of triptans

A

5HT receptor agonsits; MOA not fully known but may reduce peripheral pain signals

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24
Q

Clinical features of meningitis vs meningococcal septicaemia
Most common cause of viral meningitis

A

Meningitis = headache, neck stiffness (in some), photophobia, fever, vomiting, seizure (bacteria/virus in CSF around brain and spinal cord)
Meninogococcal septicaemia (meningococcus in bloodstream) = presence of non-blanching haemorrhagic rash
Viral meningitis - enteroviruses like coxsackie

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25
Q

Investigations for meningitis in hospital (3 main ones)

A
  1. Lumbar puncture- CSF analysis (culture, neutrophils, glucose, protein, PCR)
  2. Blood glucose (to compare against CSF glucose)
  3. Bloods - Meningococcal PCR (quicker than culture)

note neutrophils suggestive of bacterial meningitis rather than other causes like HSE.

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26
Q

Community vs hospital management for meningitis?

A

Community - suspected meningitis + non blanching rash–> start Benzylpenicillin and immediate transfer to hospital.
Hospital
- abx as per trust guidelines and dependent on age
+/- steroids dependent on LP results
- fluids and cerebral monitoring

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27
Q

Abx treatment for bacterial meningitis; how does it vary for children <3 months?

A

<3 months: Cefutaxime + Amoxicillin (to cover for listeria contracted during pregnancy)
>3 months: Ceftriaxone (because Cefutaxime can cause dangerous increase in bilirubin)

or according to local guidelines

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28
Q

Secondary causes of headache - intracranial (list 5), extracranial (list 5)

A

Intra = meningitis, haemorrhage (SAH/ICH) venous sinus thrombosis, temporal arteritis/GCA, raised ICP
Extra = acute angle closure glaucoma, pre-eclampsia, encephalitis, carotid artery dissection, sinusitis

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29
Q

Raised ICP: presentation & examination findings

A

Presentation: worse in morning with coughing & bending. Nausea & vomiting. Reduced GCS. Visual disturbance/neurological syx/seizures.
Examination: Reduced GCS. Pupil dilation. Papilloedema. CN III palsy (late). Cushing’s (if herniated). Cheyne Stokes respiration.

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30
Q

Herpes simplex encephalitis is most common cause of sporadic encephalitis.
The virus typically affects which lobes, causing which typical symptoms?
Ix: CT head & LB. Findings?
Mx?

A
  • Temporal lobes
  • Headache, fever, seizure
  • Focal sx - aphasia
  • CT - Hypodensities/ptetchial haemorrhages in temporal lobes (aka bitemporal lobe changes)
  • LP - raised WCC & proteins.
  • IV Aciclovir
31
Q

Risk factors for venous sinus thrombosis?

A

Hypercoaguable state (pregnancy)

32
Q

Venous sinus thrombosis - presentation, investigations & management

A

Presentation: headache, N&V, seizures, features of raised ICP, focal neurology.
Investigations: CT venography
Management: LMWH + antibiotics (high risk of infection)

33
Q

GCA presentation, investigations(3) and managementy - how does this vary for if there is visual involvement?

A

Presentation: over 55, temporal headache, scalp tenderness & jaw claudication, ipsilateral blindness, papilloedema.
Investigations:
1. Bloods - raised ESR,
2. Duplex temporal artery - (assess speed and volume of blood) - “halo” sign, stenosis
3. Biopsy temporal artery - multinucleated cells/skiplesions
Management: high dose glucocorticoids
Evolving visual defect: Methylpred then Pred
No visual defect: Pred

34
Q

Primary causes of headache

A

Tension headache
Cluster
Migraine

35
Q

Typical presentation of neurogenic thoracic outlet syndrome?

A

Pressure on bracchial plexus –> wasting of thenar eminence, hand weakness (worsened by raising above head), +/- paraesthesia +/- autonomic symptoms

36
Q

Typical presentation of vascular TOS?

A

vascular: pressure on subclavian artery or subclavian vein.
Artery - claudication.
Vein - arm swelling.

37
Q

Features of Tremor
* Parkinsonism
* Benign Essential Tremor
* Cerebellar disease
* Anxiety
* Thyrotoxicosis
* Hepatic encephalopathy
* CO2 retention
* Renal failure (uraemia)

A
  • Asymmetrical, resting tremor (“pill rolling”), relieved by voluntary movement. Associated with bradykinesia / problems with dexterity/fine movement
  • Symmetrical, alleviated by alcohol and rest, worse if arms outstretched.
  • Intention tremor, impaired finger-nose test.
  • Symmetrical, worse under stress. Hx of MH.
  • Associated with thyrotoxic signs
  • Asterixis (flapping tremor) - bilateral, postural. Hx of CLD.
  • Asterixis (flapping treor) - bilateral, postural. Hx of COPD.
  • Same
38
Q

Motor Neurone Disease
* brief definition
* subtypes, relative prognosis and whether UMN/LMN signs are affected (4)
* risk factors (3)
* sx presentation and important negatives (3)
* only licensed treatment available:

A
  • MND is a neurodegenerative condition twhich ultimately results in paralysis.
  • ALS (50% of cases, both UMN/LMN sx, 2-5 yr prog)
  • PMA (7-8yrs, LMN)
  • PLS (10 yrs, UMN)
  • PBP (<1 yr, both)
  • Genetics (10%), idiopathic, physical activity, male, increasing age
  • Progressive muscle weakness or bulbar symptoms. Negatives - spares ocular & pelvic floor muscles - x oculomotor disturbance, x incontinence - until late stage.
  • Riluzole (glutamate antagonist)
39
Q

Distinguish bulbar palsy from pseudobulbar palsy

A

Both affect the cranial nerves 9,10,11,12 found on the medulla of brainstem - involved in function of muscles of face, mouth and tongue. Both cause tongue muscle wasting +
* Bulbar palsy- LMN signs - fasciculations
* Pseudobulbar palsy - UMN - exaggerated jaw jerk relfex, tongue spasticity

40
Q

Multiple scerlosis
* Definition
* Disease patterns (4)
* Risk factors (3)
* General presentation, and common types (3)
* Diagnosis (2) and investigations (2)
* Management - MDT & Neuro rehab team. Long term treatment class and medx for relapse
* First line treatment options for spasticity (2)

A
  • A chronic progressive condition caused by demyelination and plaque formation of the CNS neurons. Often autoimmune attack against the myelin sheath.
  • Clinically isolated episode (technically not MS yet)
  • Relapsing-remitting (most common)
  • Secondary progressive (R/R then continue progressing)
  • Primary progressive (without R/R)
  • Female sex, EBV, genetics, smoking, obesity
  • present with variable sx depending on which part of CNS is affected (5 - motor, sensory, visual, cerebellar, autonomic)
  • Based on CNS lesions “disseminated in time & space & greater than 1 yr in nature.
  • MRI Brain & spial cord - plaques.
  • LP - oligoclonal bands (antibodies) in CSF.
  • DMARDS
  • Corticosteroids for relapse (Methylpred)
41
Q

Multiple-sclerosis: management
To reduce relapse: DMARDS
- types and general mechanism
To treat relapses: croticosteroids
- type
- Symptomatic treatment
- treatments for 5 main symptoms
Conservative
- Exercise, weight loss, smoking cessation
- (physio, OT)

A
  • Fingolimod (S1P modulator) and Natalizumab (anti-A4B1) - biologic therapy- target specific leucoytes/interleukins to reduce immission.
  • Methylprednisolone
    *- Limb spasticity - Baclofen/Gabapentin & physiotherapy
  • Fatigue - Amantine & CBT
  • Depression - SSRIs & CBT
  • Urge incontinence - anticholinergics
  • Neuropathic pain - Amitryptiline/Gabapentin
42
Q

Visual effects
- Optic neuritis (3 key sx, examination finding?, cause other than MS)
- Internuclear opthalmoplegia
- Conjugate gaze palsy (CN 6)
- Double vision
- Uhthoff’s

A

Optic neuritis
1. **Visual **- cloudy vision, red desaturation, central scotoma
2. Pain - worse on mvmnt
3. RAPD
4. O/E - papilloedema
Cause - MS, syphillis, autoimmune conditions (SLE, DM), viruses (measles, mumps)
INO
damage to medial longitudinal fasciculus between CN3 (oculomotor) and CN6 (abducens)
- inability to adduct affected eye and horizontal nystagmus of opposite eye
Conjugate gaze palsy
inability to both both eyes together in straight line
Double vision
noted on H test (CN I)
Uhthoff’s
visual changes are worsened by rise in body temp

43
Q

Internuclear opthalmoplegia

A
  • Demyelination or any damage to the MLF - medial longitudinal fasciculus (connection between CN3 and CN6)
  • inability to adduct eye of affected side and nystagmus of other eye
44
Q

Transverse myelitis
-definition; trigger
- symptoms below the level of the cord?
- L’hermitte’s sign?
- treatment

A
  • Focal inflammation extending across the spinal cord - triggered by infectious or autoimmune process
  • Motor and sensory sx below level of cord
  • E.g. L’hermitte’s sign = sensory dissturbance (electric shock down back of neck/back - due to demyelination within cervical spinal cord) and tight-band sensation around trunk
  • Dexamethasone
45
Q

Wet, wobbly & wacky
(urinary incontinence, recurrent falls and dementia) is the classical triad for what?
What causes it?
Risk factors?
What therefore would you not expect?
Typical finding on cxr - or not a finding?
Mx?

A

Normal pressure hydrocephalus
* reversible dementia
* reduced absorption of CSF at the arachnoid villi –>progressive fluid build-up in brain -> develop sx over few months as large ventricles obstruct brain tissue
* increasing age, head injury, stroke, CNS infection
* x papilloedema/raised ICP
* cerebral imaging shows ventriculomegaly with lack of sulcal enlargement (aka ventricles are bigger but not causing raised ICP)
* mx - ventriculoperitoneal shunt

46
Q

Gait abnormalities - cause, features
* Hemiplegic
* Diplegic
* Parkinsonian
* Ataxic
* Neuropathic
* Myopathic
* Antalgic

Involuntary movements
* Choreiform
* Akathitosis
* Ballismus

A
  • Circumduction. UMN lesion (e.g. stroke) - spastic weakness of lower limbs.
    Scissoring. (overlapping of lower limbs). Bilateral CVA (stroke), spinal cord lesion, MND.
  • Shuffling –> festinant gait w slow initiation, reduced stride length, reduced arm swing, and stooped posture. PArkinson’s disease/PD+/drugs/viral.
  • Broad based staggering. Problem with balance: cerebellum, vestibular system or proprioception. E.g. alcoholic cerebella dysfunction, labrynthitis, sensory ataxia from spinl cord lesion/DM.
  • High steppage foot drop/toe dragging. - weakness in distal muscles due to peripheral neurapathy. Common peroneal neuropathy (L4,L5,S1) - e.g. L5 radiculopathy or polyneuropathy/CMT.
  • Waddling; weakness of hip abductors (minimus/medius). Pelvis dips on unsupported side. Positive Trendelenberg.
  • Abnormal gait due to pain - e.g. #, osteoarthritis, RA.
  • Chorea - Involuntary dance-like movements. Huntington’s/Sydenham’s.
  • Athetosis - slower form of chorea - continuous, writhing movements (“without position)
  • Ballismus - severe form of chorea - with violent flinging of limbs
47
Q

Intracranial venous thrombosis: includes sagittal sinus, cavernous sinus thrombosis and lateral sinus thrombosis. It can result in a stroke/CVA.

  • risk factors
  • presentation (signs of raised ICP)
  • ix and typical finding if sagittal sinus thrombosis
  • mx
A
  • hypercoaguable state, smoking
  • headache, N+V, LoC
  • MRI venography: “empty delta sign”
  • anti-coagulants: LMWH
48
Q

Intracranial hypertension
- risk factors
- presentation
- ix
- mx - lifestyle and medical

A
  • fenale sex, obesity, COCP use, pregnancy, other drugs
  • headache worse on bending forward, signs of raised ICP, papilloedema, enlarged blind spot
  • MR venogram: “Empty sella sign”
  • Weight loss
  • Acetazolamide to reduce production of CSF
  • +/- topiramate (also beneficial for weight loss)
  • surgical options e.g. ventriculoperitoneal shunt
49
Q

Parkinson’s plus syndromes
- Multisystem atrophy (3 main features)
- Dementia with lewy bodies (distinction from PD)
- Progressive supranuclear palsy (PSP)
- Corticobasal degeneration
Other causes of parkinsonism:
- Drugs
- Infection - viral
- Wilson’s disease
- Trauma
- Toxins

A
  • basal ganglia (PD), cerebellum (ataxia) and autonomic dysfunction
  • cognitive decline prior to motor symptoms and often fluctating congition +/- visual hallucinations
  • PSP: impaired vertical gaze, instability/falls, parkinsonism, cognitive decline
    *
50
Q

Parkinson’s medication
1st line:
Levodopa
- medicinial forms - what else is co-prescribed and why?
- side effects
2nd line or 1st line if motor symptoms aren’t main problem
Example:
- Dopamine agonists
- MAO-B inhibitors

Adjuncts:
- Antimuscarinics
- COMT-Inhibitors

A

Levodopa
- Addition of a decarboxylase to prevent breakdown of dopamine before it reaches the brain
- Co-beneldopa (Levodopa and Benserazide)
- Co-careldopa (levodopa + Carbidopa)
- ses: dyskinesias
Dopamine agonists
- Bromocriptine
- Pergolide
- Carbergoline
MAO-B inhibitors
- Rasagline
- Selegiline

Adjuncts
COMT-Inhibitors
…capones
Antimuscarinics
to help DIP primarily for tremor and rigidity
Procyclidine
Benzotripine etc

51
Q

Bell’s palsy; cranial nerve 7 palsy
* Risk factors
* Presentation
* Management

A

Risk factors:
- Pregnancy
- 20-40yrs
- ? herpes simplex infection
Px - Sudden onset of
- Ipsilateral paralysis of face including forehead (LMN)
- Hyperacusis/ear ache (facial nerve supplies stapedius muscle)
- Loss of taste (CN VII- anterior 2/3 of tongue)

Mx:
- Prednisolone PO within 3 days
- Eye care (tape closed at night, artificial tears ifn necessary)
-

52
Q

Herpes simplex encephalitis
- typically affects which lobes?
- typical causative organism?
- Presentation
- Investigations (LP), viral PCR, CT/MRI Brain, EEG - findings
- Mx

A
  • temporal lobes
  • HSV type 1
  • meningism, seizures, coma
  • LP: raised lymphocytes, normal protein, normal glucose
  • CT: ptechiae, MRI brain - hyperintensity of temporal lobes, EEG - lateralised periodic discharges at 2Hz
  • IV Aciclovir
53
Q

Myasthenia gravis
Autoimmune condition of the NMJ, autoantibodies to acetylcholine receptor on post synaptic cleft of NMJ
- Presentation
- Fatiguability in muscles can be eliicited by (3)
- autoantibodies (most likely to least)
- ix name
- Positive test if ….
- additional ix if thymoma suspected (strong link)
- mx (2)
- if initial treatment not effective consider
- differentials

A
  • faceFacial/oculomotor problems - ptosis, diplopia, dysarthia, dysphagia;
  • limbsProximal limb weakness; fatiguability
  • prolonged blinking –> ptosis; prolonged upward gazing –> diplopia, repeated arm abduction –> unilateral weakness
    autoantibodies - anti: ACH-R (85%) antiMUSK (muscle specific tyrosine kinase antibodies)
    Ix
  • single fibre electromyography: high sensitivity (>92%)
  • CT/MRI thorax - thymus
  • Edrophonium test / or neostigmine: IV dose of antiacetylcholinesterase enzymes (blocks breakdown of Ach)
  • positive if symptoms improve (temporary rise in ACh at NMJ relieves weakness)
    Mx
  • reversible acetylcholinesterase inhibitors - Pyridostrigmine/Neostigmine & immunosuppression eventually - reduce production of autoantibodies (Prednisolone, Azathioprine etc)
  • ?mABs - Rituximab
  • thymectomy
  • Lambert-Eaten syndrome (NSCLC; squamous), cranial nerve III palsy, Guillan Barre syndrome/Miller Fisher syndrome starts in eyes, myopathy, muscular dystrophy (in MG the CK level is normal unlike in the latter)
54
Q

What triggers a myasthenic crisis?
What are patients at risk of?
Treatment (2)

A
  • Infection, stress, trauma, menstruatiom
  • Respiratory failure due to weakness of resp muscles
  • Iv IGs or plasma exchange (plasmapharesis)
  • +/- NIV if severe
55
Q

Muscular dystrophies - genetic conditions causing gradual muscle weakness/wasting
- Paeds: Duchenne’s/Becker’s
- Adults: Myotonic dystrophy
- Other rare forms …..

Duchenne’s/Becker’s
- genetic inheritenace of both
- mutation on gene Xp21 which codes for?
- which is the more severe form?
- Ix - raised CK; definitive diangosis by?
- Mx -??
- Associated with which condition

Duchenne’s
- Presentation and age of onset
- positive sign on examination
- signs other than myopathy

Becker’s
- key distinguishing points (2)

A
  • X-linked recessive
  • Dystrophin - endodess for msucle protein
  • Duchenne’s: frameshift mutation; becker’s - non frameshift
  • Duchenne’s at 5, becker’s at 10
  • Genetic testing; definitive
  • Steroids to slow progression and creatine supplements
  • poor prog, most cannot walk by age 12
  • dialted cardiomyopathy

Duchenne’s
- Gower’s sign positive = use arms to stand from squat
- Calf psuedohypertrophy
- progressive proximal muscle weakness from age 5
- intellectual impairment may be present

Becker’s
- develops after 10 years
- rarely have intellectual impairment

56
Q

Myotonic dystrophy
type of inhertied muscular dystrophy more common in adults (2 types)
- characterising features
- on examination
- associated with which ocular condition (req opthalmoscope)

A
  • myotonia and slurred speech (myotonia of pharyngeal/oral muscles)
  • on clenching fist and opening it, slow muscle relaxation
  • normal sensation, normal reflexes
  • symmetrical weakness proximal>distal
  • cataracts
57
Q

Polymyositis: DOE
- requires ruling out other causes of myopathy (endocirne, electrolyte, toxic etc)
It is an inflammatory myositis due to underlying causes - autoimmune, infection, drugs (statin), CTs
- what cancers is dermatomyositis associated with?
- Bloods - what is raised?
- Diagnosis obtained from..?
- Mx

A
  • ovary,GI,breast
  • CK raised
  • muscle biopsy
  • steroids
58
Q

**Subacute combined degeneration of the cord **
- Causes
- Presentation (3)
- SAD therefore
- Like MS it can also cause which sign on neck flexion?
- Typical example patient

A
  • Vitamin B12 (pernicious anaemia) or Vitamin E deficiency - degeneration of the spinal cord due to demyelination
  • spastic paresis, bilateral- UMN signs below level of cord (x corticospinal) - (but note can have absent ankle reflexes - doesn;t fit with rest)
  • loss of vibration/proprioception, bilateal ( xdorsal columns)
  • Ataxia, bilateral Romberg’s +ve
  • SAD - still in pain (spinothalamic intact)
  • L’hermitte’s sign
    Post-Chron’s op, presenting with paraesthesia in toes and fingers, clumsiness and ataxia
59
Q

Friedrich’s ataxia
most common inherited form of ataxia, presents similarly to SADCD
- General presentation
- Affects what other system due to mitochondria dysfunction?

A

-Spastic paresis, ataxia, and loss of vibration/proprioception
- also note INTENTION TREMOR
- NS, heart and pancreas

60
Q

Central cord syndrome
- cause
- presentation

A
  • hyperextension of neck, e.g. car injury
  • most common form of incomplete cord lesion
  • Bilateral spastic paresis UL>LL
  • +/- sensory involvement
61
Q

Complete spinal cord lesions have no function below site of injury. Incomplete have some function (motor/sensory) below site.
Types of incomplete spinal cord lesion (4)

A
  • Brown-Sequard (unilateral signs)
  • Central/cervical cord syndrome
  • Anterior cord syndrome
  • ## Posterior cord syndrome
62
Q

Anterior cord syndrome
- caused by
- sx
- presentation (motor and sensory deficit)

A
  • Anterior spinal artery occlusion (aortic dissection, sudden disc rupture, tumour compression etc)
  • chest/back pain and spinal shock
  • Bilateral spastic paresis and bilateral loss of pain/temp sensation
63
Q

Syringomyelia
- CSF filled cyst in the spinal cord. Starts medially in cord and then expands outwards.
- Treat cause of syrinx or shunt.
- Risk factors
- Presentation

A
  • Chairi malformation (cerebellar herniation); tumours, trauma, meningitis
  • Cape-like distribution of loss of pain/temp sensation (superheroes feel no pain) damage to spinothalamic tract
  • ## Spastic weakness LL>UL
64
Q

Neurosyphillis: what is tabes dorsalis

A
  • wasting of the dorsal columns
  • loss of proprioception/vibration sensation
65
Q

Degnerative cervical myelopathy
Risk factors
Presentation
What is Hoffmann’s sign?
Investigation and finding
Mx - requires urgent insput from..
Definitive surgery
Differentials (2)

A
  • Smoking, genetics, occupation (high axial loading)
  • Neck or limb pain
  • Loss of motor function +/- sensory/autonomic sx
  • Impaired gait and balance

E.g. neck pain, loss of digital dexterity and clumsiness
- MRI Spine- disc degeneration and ligament hypertrophy
- Urgent neurosurgical assessment
- Decompressive surgery
Differentials
- Carpal tunnel syndrome
- Cervical disc prolapse

66
Q

Cerebellar syndrome
- Symptoms (DANISH)
- Causes

A

Symptoms
Dysdiadokinesia
Ataxia
Nystagamus (horizontal)
Intention tremor, impaired finger-nose test
Slurred staccato speech
Hypotonia, impaired heel-shin test
Causes
- Friedrich’s ataxia (most common hereditary cause: ataxia, spastic weakness, impaired dorsal columns + intention tremor. Affects heart & pancreas too)
- SACDC (ataxia, bilateral spastic weakness [UMN], impaired proprioception/vibration sense)
- Alcoholic liver disease
- Multiple sclerosis
- Pareneoplastic (lung cancer)
- Drugs: phenytoin, lead poisoning
- Cerebellar stroke
- Cancer - cerebellar haemangioma
- Ataxic telangectasia
- Multisystematrophy (parkinson’s plus syndrome)

67
Q

Brain abscess
May be caused by sepsis from middle ear/sinuses, trauma/surgery to scalp, penetrating head injury or embolism (endocarditis).
Presenting sx depend on site of abscess -other general signs:
Ix -
Mx - surgical and abx following

A

Px - fever, raised ICP signs (papilloedema, nausea, seizures), focal neurology, headache (dull, persistent)
Ix - non-contrast CT head
Mx - craniotomy + debridement
IV Abx - Cephalopsorin + Metronidazole
Manage raised ICP - Dexamethasone

68
Q

Facial nerve palsy
Supply - face, ear, taste, tear
Face - muscles of facial expression (motor)
Ear - nerve to stapedius (causing hyperacusis, ear pain)
Taste - supplies anterior 2/3 of tongue
Tear - paraysympathetic fibres to lacrimal glands
Causes of bilateral facial nerve palsy? (4 main)
Causes of unilateral?

A

Bilateral
- Sarcoidosis
- GBS
- Lyme disease
- Bilateral acoustic neuroma (Neurofibromatosis type 2)
- Bell’s (unlikely)
Unilateral
LMN - all include forehead
- Bell’s
- Ramsay hunt (VZV)
- Parotid tumour
- MS
- HIV
- DM
UMN
- stroke (forehead sparing)

69
Q

TIA: sudden onset focal neurology caused by brain, spinal cord or retinal ischemia, without acute infarction (generally features resolve in 1hr
Managenent;
1. Immediate antithrombotic
2. Specialist review with stroke team - urgent (criteria x3?)within 24hrs or within 7 days

Ix - recommend CT ehad not done unless clinical suspcion of alternative diagnosis. What is the preferred method ofimaging if required - same day or at specialist assessment?
Further management? Like stroke

A
  1. Aspirin 300mg (unless bleeding disorder, on anticoagulant/low-dose aspirin anyway, contraindications)
  2. Urgent if suspected cardioembolic source/severe carotid stenosis/crescendo TIA.
    Review within 24hrs if suspected TIAin last 7 days, otherwise if longer can be seen wtihin 7 days

Imaging: MRI diffision weighted
Others: carotid imaging - doppler
Further management: anti-platelet (clopidogrel or aspirin & dipyridamole) and statin (atorvastatin 20-80mg daily)

70
Q

Brain tumours
* Presentation
* O/E - fundoscopy signs for raised ICP

A

Progressive focal neurological symptoms, signs of raised ICP and systemic signs, altered mental state, focal seizures.
Papilloedema= swelling of the optic disc, elevtated optic disc, haemorrhages, Paton’s lines (folds in retina around optic disc), engorged retinal veins, loss of venous pulsation

71
Q

Types of brain tumour
1.Gliomas (arise from glial cells in brain/SC) - 3 main types from benign to most malignant:
2. Meningiomas (arise from meningeal cells): effect?
3. Pituitary adenomas(arise from pituitary gland) can be secretory/non-sec. Sx due to hormone excess? (Or depletion):
4. Vestibular schwannoma/acoustic neuroma: Nerve origin, location, association

A

Gliomas:
1. Ependymoma
2. Oligodendroglioma
3. Astrocytoma - most common/aggressive is glioblastoma
Meningiomas:
- Generally benign
- Mass effect rather than invasive
Pituitary adenoma
1. Cushings (excess cortisol)
2. Acromegaly (excess GH)
3. Hyperprolactinaemia (excess prolactin)
4. Thyrotoxicosis (excess TSH, thyroid)
Vestibular schwannoma
- CN 8 (vestibulocochlear)
- cerebellopontine angle
- unilateral s/n hearing loss, tinnitus, dizziness +/- facial nerve palsy (compression on CN7)

72
Q

Stroke mx
- Initial
- Intervention
- 2ndary prevention

Stroke & AF mx
-secondary preventiON
- how soon after stroke should this be started

A

Initial Aspirin 300mg stat (continue 2 weeks)
Intervention - thrombolysis - alteplase if within 4.5 hours of onset, thrombectomy - if last well between 6-24hrs ago, or if past 24 hours - bot (and if PCA/basilar artery or potential to salvage brain tissue)
2ndary prevention: antiplatelets; lifelong
1. Aspirin & dypridamole
2. Clopidogrel 75mg
+ Statin (atorvastatin after 48hrs)

If stroke + AF –> secondary prevention with anticoagulants, e.g. DOAC or Warfarin: apxaban AFTER 2 WEEKS

73
Q

Malignant spinal cord compression
- oncology emergency
- extradural compression from tumour on spinal cord (lung, breast and prostate most common)
- features
- urgent investigation within 24hrs
- management
- urgent oncology assessment for consideration of:

A
  • Back pain
  • Neurological signs - increased reflexes below lesion, reduced at level of lesion.
  • Paraesthesia and lower limb weakness
  • Urgent MRI Spine
  • High-dose Dexamethasone oral
  • Consideration for radiotherapy or surgery

Year 4/5 Revision (21 decks)

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