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PACES 2021 > Neuro > Flashcards

Neuro Flashcards

1
Q

Causes of Stroke

A

Ischaemic- emboli or atheroscleroti

Hemorrhagic- Intracerebral haemorrhage
SAH
SDH
EDH

Venous

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2
Q

RFs for CVA

A 
Smoking
HTN
dm
af
Previous TIA
Carotid artery stneosis
FH 
OCP
ETOH
Obese
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3
Q

Bamford Classication

A 
Lacunar stroke= any of
Pure motor hemiparesis
Pure sensory hemiparesis
Ataxic hemiparesis 
Sensori motor stroke

TACI (Total anterior circulation infarct)-
3 or 3
1) Higher cerbreal dysfunction
2) Homonymous field defet
3) Ipsilateral motor defect of two regions (of face, arms and legs)

PACI (Partial anterior ciruclation infarct)
2 or 3

Posterior circulation infarct
One of….
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

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4
Q

Difference between ACA and MCA strokes

A

ACA= Affects legs over arms- more likely to have urinary incontinence

MCA= Weakness of arm and face over legs
Expressive or receptive dysphasia if dominent hemisphere
Quadrantiopia depending if parietal (floor) or temporal (sky) lobe affected
Other cortical signs including
a) Sensory cortical impairment- 2 point discrimination, unable to recognise from touch and agraphaesthsia
b) Dominent parietal lobe- sensory cortical features plus auditory agnosia, Gerstmann syndrome (inability to calculate, read or write, finger agnosia and loss of left-right discrimination)
c) Non dominant parietal lobe- hemi neglect, apraxias (e.g in dressing or gait)

(View like structure of blood supply to brain!)

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5
Q

Posterior Circulation infarct syndromes

A 
1) PICA syndrome (Wallenberg's)
Ipsilateral pain and pinbrick impairment to face and contralateral trunk and extremity pain and pinprick
Dysphagia hoarsenss and logg of gag
Vertigo,nystagmus
Ipislateral cerebellar signs

Aka CN 8-10 and cerbellar

2) AICA syndrome (Lateral pontine- Unwellenberg’s)
Ipsilateral sensory impariment of face and contralateral trunk
Paralysis of ipsilatreal muscle sof mastication and paralysis of face (LMN)
ipsilateral hemiataxia

So affects CN 5+7

3) PCA occlusion- contralateral homonymous hemianopia with macular sparing
Contrlateral pain and temp loss
Memory deficits
Cortical blindness and hemineglect

4) Weber’s syndrome (3rd nerve palsy and contralateral hemiplegia due to infarct of medial midbrain

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6
Q

Investigation of stroke

A

Identify timing of stroke regarding thrombolysis

Baseline obs, CBG, BP and 12 lead EG.
Baseline bloods- FBC, Clotting, TFTs, LFTs and ANA
Hba1c, Lipid profile
CT head- may do CT angio if considering thrombolysis or thrombectomy

Alongside this- SALT
MRI head
24 hour tape
TTE
Carotid dopplers

If young want to investigate for thrombophilias and inflammatory causes

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7
Q

Management

A

If caught in first 4.5 hours then thrombolysis
May also consider thrombectomy

CI to thombolysis= previous ICH
Active internal bleeding or previous GI bleed, liver disease or varices.
Surgery in last 14 days
BP >185/110
Stroke or head injury in last 3 months.

If non haemorrhagic then want to give loading aspirin- switch to clopidogrel or DOAC depending on evidene of AF
Start statin and treat BP and DM if diagnoses

If Carotid artery >70% stenosed then carotid endarterectomy.

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8
Q

SAH summary

A 
RFs- FH, APCKD, Ehlers Danlos
Marfan's
Smoking
HTN
Drugs e.g cocain
IE with mycotic aneurysm

Classical features

Complications- Vasospasm most often around 4-10 days. Treat with Mifedipine.
Hydrocephalus-
Rebleeding
Seizures
Pulmonary oedema
Cardiac arrythmias
Hyponatraemia (SIADH or salt wasting)
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9
Q

Ddx of stroke

A

SOL e.g tumour or abscess or parasite
Viral encephalitis
Neuroinflammation- MS, neurosaroid, Bechet’s
Todd’s paresis
Migraine
Stroke mimic on old stroke when otherwise unwell

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10
Q

Multiple Sclerosis Clinical features

A

Can affect nearly any part of the CNS
Optic neuritis- pain on movement, reduced acuity and olour desaturation
Diplopia due to INO
Spinal cord syndrome- urinary/bowel dysfunction, sensory dysfunction or paraparesis
Motor involvement later in disease with weakness and spasticity
Cerebellar signs
Dysarthria, vertigo
Lhemmitte’s sign- electricla sensation from neck to limps on flexion
Uhthoff’s phenomen- worsening of symptoms on rise in body temp)

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11
Q

Classification

A

Relapsing-remitting MS- 85%
Secondary progressive MS- can develop from relapsing remiting
Primary progressive MS

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12
Q

Investigations in MS

A

MRI head and Spine
Basic blood tests to rule out Ddx
Visual and auditory evoked potential to demonstrate old lesions
CSF may show oligoclonal bands

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13
Q

Management of MS

A

Acute episode- IV methyprednisolone
Screen and treat any systemic infections

Get neurologist involved for diagnosis and management

Symptomatic management- MDT approach= PT/OT/SALT
Antispastmodics
LT catheter or intermittent self catherisation
Laxatives
Treat pain, swallow, depression, sexual dysfunction

Disease modifying therapy- Beta interferon and glatiramer can be used (SEs- flu like symptoms, AI hepatitis, and failure to be efficacious)
Natalizumab- mab against adhesion molecule on T cell
Alemtuzumab Anti cd52
Fingelomod- oral agent for highly active mS

All mainly used RRMS

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14
Q

Neuromyeltitis optica

A

Demyelination of spinal cord and optic nerves
Have a more extensive lesion sthen in MS and often extends over 3 vertebral segments.
Due to Antibody against aquaporin 4

Responds to IV iG and plasma exchange in short term event
Steroids and immunosuppression in long term

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15
Q

Parkinson’s disease signs

A 
Walking aids/anti parkinsons medications
Hypomimic facies, siallorhoea,
Classic cait, reduced arm swing and difficulty turning
Asymmetricla tremor, worse on distraction 
Bradykinesia
Lead pipe rigiity and cogwheel rigidity
Quiet monotonous speech
Micrographia
Impaired sense of smell
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16
Q

Causes of Parkinsonism

A 
Idiopathic PD
Drug induced (neuro-epileptis and anti emetics)
Parkinson's plus- Progressive suprnuclear palsy, MSA and corticobasal degeneration
Dementia wiht Lewy bodies
TOxins- MPTP, manganese
Wilson's disease
Post trauma
VASCULAR PARKINSONISM
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17
Q

Treatment of Parkinson’s disease

A

Involve neurology team and Parkinson’s nursing team

L-dopa 
Dopamine agonists
Monamine oxidases inhibitors 
COMT inhibitors 
Amantadine 
Anticholinergics
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18
Q

Cerebellar disease Symptoms

A

DANISH

Dysdiadochokinesis-
Ataxia
Nystagmus
Intention tremor
Staccato speech
Hypotonia/hyporeflexia

Will also have rebound phenomenon and ataxia on gait and truncal

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19
Q

Causes of Cerebellar disease

A 
Demyelination- MS
Alcohol
SOL
Parneoplastic
Stroke (Ischaemic) 
Hypothyroidism
Drugs e.g phenytoin 
Metabolic- B12 or copper (Wilson's)

Genetic causes include spinocerebellar ataxia and fredrich’s ataxia

20
Q

Spinocerebellar ataxia

A

Large range of subtypes of spinocerebellar ataxias

AD and can have extrapyrimidal sings, peripheral neuropathy and opthalmoplegia

Fredrich’s ataxia- has peripheral neuropathy, spasticit, diabetes and deafness. Wheelchair bound often
Demonstrate anticipation!

ATAXIA TELANGIECTASIS- SKIN AND EYE TELANGIECTASIA AND DYTONIA. ar INHERITENCE

21
Q

Spinal Cord disorders- clinical findings

A

Spastic gait
Spasticity in lower limbs (increased tone) and clone
Reduced power- (Extensors worse then flexors in arms, flexors worse then extensors in legs)
Hyperreflexia
Sensory level above L1
Catheter in situ
Spinal surgery scars

22
Q

Classification of spinal cord disease

A

1) Vascular- Occurs within minutes.
Such as Anterior spinal artery infarction or AVM
Anterior spinal infarction will spare dorsal column sensation

2) Compressive- Hours to days. Often asymmetrical.
Predominantly motor but can affect sensory systems
Include- Degenerative disease- e.g disc herniation
Malginancy- both mets, and intermedullary or extramedullary
Trauma
Abscess

3) Infective- Hours
Often more painful and associated fevers
Can be bacterial- e.g Staph, strep, TB
Or viral, HIV, enterovirus, Herpes and HTLV

4) Inflammatory- Hours to days
Such as due to MS, SLE, sarcoid or vasculitis

5) Nutritional/metabolic- Days to weeks/months
Such as B12 decifiency or copper deficiency
Associated with loss of dorsal column sensation

6) Neurodegenerative and congenital-

Several different conditions within these. Occur over months-years

Key example is hereditary spastic paraperesis- have increased tone and spasticity with reflexes but persevered power

Can also occur in Fredrich;’s ataxia and spinocerebellar disease.

23
Q

Investigations

A

MRI spine
Blood tests and markers for infection/vasculitis if concerned
Vit B12 too and HIV test
MR angiogram if thinking vascular cause.
If thinking MS then concurrent visual and auditory evoked potentials for previous episodes.

24
Q

Bulbar and pseudobulbar palsy

A

To examine use- Bbb for lips, ttt for tongue, kkk for palate

Bulbar palsy is LMN lesion- Have nasal speech and fasciculations and wasting of the goneu

Caused by MND , myasthenia gravis, myopathy

Pseudobulbar palsy is UMN lesion-
Have spastic hoarse voice and slow tongue
Linked to brisk reflexes in jaw

Causes MND, MS and brainstem stroke

25
Q

Causes of Mixed UMN and LMN signs

A

1) Cervical radiculopathy
2) MND
3) Subacute degenration of the cord
4) Syringomyelia

5) Conus meddlaris compression- as per classic cauda equina. Will have sphincter disturbance, sensory level and weakness assocaited
Plus saddle anaesthesia.

26
Q

Signs of cervical radiculopathy

A

Wasting of arm muscles- if C5-C6 then of biceps and supinators
If c8-t1 then small msucles of hands

Brisk reflexes belown lesion
Pain localised to neck in radicular pattern
Sensory loss localised to radicular patten

27
Q

Motor Neurone disease- signs and management

A 
Mixed picture
Will can have reduced or spastic tone
Reduced power
Brisk or absent reflexes
Fasciculations- diagnostic

Sensation will remain intact

Subtypes include- Amyotrophic lateral sclrosis- Classic picture affects UMN and LMN of limbs and bulbar system
If only bulbar then is progressive bulbar palsy

primary lateral sclerosis- Only UMN signs
Progressive muscular atrophy- only LMN signs

Dx- is by EMG demonstrating widespread denervation

Mx- Supportive
MDT in put for symptom control and optomisation
PT/OT/SALT- may need PEG
Riluzole will prolong lifespan by 3 months
May need NIV if T2RF due to neuromusclar weakness

28
Q

Syringomyelia

A

Fluid filled cyst in central spinal cord- linked to tumours and arnold chiari malformation

Signs - Loss of pain and temperature sensory loss but but not touch or vibration or position.
Described as cape like as affects arms and thorax but not legs

May have scars from burns and cuts not recognised
Wasting and weakness of small muscles of hands
Brisk lower limb reflexes and upgoing plantars
May have Horner’s syndrome

29
Q

Subacute degeneration of the cord

A

Signs
Brisk knee jerks, absent ankles
Symmetrical sensory neuropathy. May be burning and lose touch, vibration and potision sense
Reduced lower limb power
Positive romberg’s sign
May be anaemic
May have optic atropy or dementia due to B12 deficinecy
Check abdomen for splenomegaly or previos surgery- e.g in crohn’s

Causes- Poor oral intake, Pernicious anaemia, ETOH intake and nitrous oxide abuse

30
Q

Causes of facial nerve palsy

A

UMN lesion= spares forehead due to bilateral innervation
LMN lesion= forehead will also be paralysed

Unilateral= Bell's Palsy
Ramsey Hunt syndrome
Stroke
Demyelination
SOL (CPA lesion)
Nerve infiltration e.g sarcoid
Bilateral= Bilateral Bell's palsy
Sarcoid
AI e.g GBS
Muscular dystrophy esuch as myotonic or fascioscapulohumeral
Infection such as Lyme
31
Q

Peripheral nerve root terms

A

Polyneuropathy- diffuse involvement of peripheral nerves
Mononeuropathy- involves on nerve
Mononeuritis multiplex- focal involvement of 2 or more neves.
Rsdiculopsrhy- single spinal nerve root
Plexopathy- involvement of brachial or lumbosacral plexus.

32
Q

Radiculopathy- characteristics and causes.

A

Burning tingling pain radiating down limb
Weakness and senroy loss in myotomal distribution
Loss of reflexes and moeot strength
Chronic rsdiculopsrhy- can result in atrophy and fasciculations.
T1 radiculopathy- causes Horner’s

Causes- Disc herniation 
Cervical/lumbar spondylosis
Spinal stenosis
Compression by tumour
Inflammation
Infections.
33
Q

Radiculopathy- characteristics and causes.

A

Burning tingling pain radiating down limb
Weakness and senroy loss in myotomal distribution
Loss of reflexes and moeot strength
Chronic rsdiculopsrhy- can result in atrophy and fasciculations.
T1 radiculopathy- causes Horner’s

Causes- Disc herniation 
Cervical/lumbar spondylosis
Spinal stenosis
Compression by tumour
Inflammation
Infections.
34
Q

Brachial plexopathy

A

Muscle weakness and atrophy from c5-t1
Reduced tendon reflezesensory loss often of axillary nerve.

Causes neuralgic amyotrophy
Neoplastic eg breast and lung cancer
Radiation induced
Thoracic outlet syndrome 
Iatrogenic after surgery

NB c8 lesion will cause weakness of flexor policcis Longus and extensor pollicis brevis whi h ulnar lesion won’t do

35
Q

Median Nerve palsy

A

Supplies LOAF, long finger flexors and sensation to lateral 2/3rds of palm and 3.5 fingers.

Causes
Carpel tunnel syndrome linked to other pathologies E.G Ra and acromegaly and pregnenacy And diabetes and hypothyroid
Trauma
Surgical injury

Clinical signs
Wasting of thenar eminence
Weakness of APB, oppons pollicis and lumbrical. 
Sensory loss over relaxsnf region. 
Provoked by Tinel's and phalens test.
36
Q

Ulnar nerve palsy

A 
Signs wasting of dorsal interossei
Wasting of hypothenar eminence
Clawing of 4-5th fingers 
Generalized weakness of hannd
Sensoey impairment oflvsd little and ulnar ring finger 
Innervates hypothenar muscles
Medial 2 lumbrical
Interossei
Adductor pollicis
Medial wrist flexors
Causes
Compression at the elbow e.g bone, prolonged elbow flexion and op compression
Bony deformity at evlow- fractures and RA and pagets 
Idiopathic
Variable anatomy
Diabetes
Vasculitis 
Leprosy
37
Q

Radial nerve palsy

A

Signs- weakness of wrist extension
Weaknes of finger extension.
If wrist is pasicly extended CNA then straighten fingers
Weakness of finger abduction and adductio.

If weakness of tricep relfex think lesion in axilla or c7 radiculopsrhy-

Causes- injury at elbow by fracture of dislocation
At humeral shaft fracture
At axilla due to traumatic compression fromx rutches or Saturday night palsy.

NB an intact trcieps reflex suggests lesion below spiral groove.

38
Q

Common peroneal nerve palsy

A

Signs- High stepping gait
Wasting of muscle on lateral lower leg
Weakness of dorsiflexion and eversion of foot
Sensory impairment over anterolateral aspect of lower leg

Causes- compression
Direct trauma
Diabetes 
Mononeuritis multiplex
Leprosy will have palpable thickening of nerve.
39
Q

Polyneuropathies causes

A 
Sensori-Motor= Diabetes
Nutritional (B12) deficiency)
ETOH
Drugs e.g isoniazid, metronidazole, chemotherapy agents and phenytoin
Hypothyroidism, renal failure
Infections e.g HIV and leprosy and syphillis
Vasculitis
Hereditary- Charcot marie tooth disease

Motor predominence= Inflammatory e.g AIDP, CIDP, MGUS associated.
Lead poisoing
Diabetic amyitrophy
Inherited e.g spinal muscular atrophy

Sensory- Paraneoplastic, Fredrich’s ataxia, chemotherapy

40
Q

Polyneuropathy signs

A

Glove and stocking sensory impairment
Muscular atrophy of affected areas
Reduced reflexes
Autonomic dysfunction with postural hypotension, impotence, GI changes and urinary inontinence.

Small fibre neuropathy affects temp and pin prick
Large fibre affects soft touch, vibration and proprioception

But often both affected

41
Q

Polyneuropathy investigations

A

History and complete neurological exam (All 3 parts)
Urine dip
Bloods for FBC, ESR, B12, Folate, HBa1c, tftS, u+E and LFTs

Can then move onto nerve conduction studies and EMG to characterise affected nerves
Vasculitis screen
Eletrophoresis
CXR
HIV

May do antineuronal antiboodies eg anti hu and anti Yo for paraneoplastic
CT-CAP for cause if above all negative.

42
Q

Fredrich’s ataxia

A

AR progressive ataxia. Most common inheritied ataxia in UK.
Inherited with Triplet repeat due to mutation on fraxin gene.
Is a spinocerebellar disese- symptoms hinted in the name!
Affects dorsal column

Neurologically develop a form of spastic paraparesis
Often have a wheelchair or walking aid present.
Will have increased tone
Reduced power in pyramidil distribution.
Absent ankle reflexes but upgoing plantars/clonus is characteristic
Also reduced coordination of hands and legs
And cerebellar speech
Sensation- reduced dosral column

Other features of Fredrich's ataxia
Pes cavus
Kyphoscoliosis
Deafness with hearing aids 
T1DM- so look for CBG pin pricks
Arrythmias and hypertrophic cardiomyopathy - so pacemaker may be present

Ix to cover neurological symptoms, risk fo daiebtes and cardiovascular risk too

Management will need to be MDT with relavent specialists and allied health professionals involved.

43
Q

Hereditary sensory and motor neuropathy
AKA
Charcot Marie Tooth Syndrome

A

In contrast to Fredrich’s ataxia this is a polyneuropathy!

Is AD inheritance
Subtypes include demyelinating and axonal.

On examination will find;
Wasting of distal lower limb but preserved thigh muscles (causign inverted champagne bottle apperance)
Pes cavus
Weakness in ankle dorsiflexion and toe extension
Variable degree of stocking distrubution sensory loss

Gait will be high stepping
Also wasting of hadn muscles
Palpable lateral popliteal nerve

44
Q

Causes of flaccid paralysis
Split into sections of nerves
TO guide presentation if not sure and also to help guide Ddx

A

Nerve foot- plexus- nerve- NMJ- Muscle

Nerve root= MND or polio
In between have cauda equina and compression

Plexus= Trauma, tumour or abscess affecting lumosarcral plexus but note often unilateral

Nerve- Several causes
Inflammation e.g GBS or CIDP
Infections e.g HIV 
Toxins- Lead
Metabolic- Porphyria and diabetic neuropathy 
Congenital- Charcot Marie Tooth

NMJ- Myasthenia gravia
Botulinism
Organophospahte poisoning

Muscle-Congenital myopathy- Myotonic dystrophy, Duchenne/becker's
Inflammtory- Poly/dermomyositis
Endocrine- Hypothyroid, Cushing's 
ETOH
 Electrolyte disurbances
45
Q

Causes of spastic paralysis

A

See spinal diseases. These show rough guide

Aka- break down is

1) MS
2) Cord compression (Sensory level)
3) Vascular cord injury (Sensory level)
4) Trauma
5) Cerbral palsy

Also can think of Fredrich’s ataxia
Hereditary spastic paraparesis
Tropical spastic parapresis
And also syringomyelia

PACES 2021 (8 decks)

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