Neurology Flashcards
Define dementia
A progressive neurological disorder impacting cognition → functional impairment.
Define pseudo-dementia?
Cognitive impairments 2° to a mental illness e.g. depression/anxiety
What is the clinical presentation of dementia?
PROGRESSIVE DECLINE:
1) Cognitive impairment (memory, language, attention)
2) Psychiatric changes (personality, emotional control, social behaviour, agitation, hallucinations and delusions)
What could Alzheimers disease be caused by?
Amyloid plaques + neurofibrillary tangles
What is Vascular dementia caused by?
Cerebrovascular infarcts: most commonly in the white matter of both cerebral hemispheres.
What is frontotemporal dementia caused by?
Focal degeneration of the frontal & temporal lobes due to tau protein deposition
What is Lewy body dementia?
Lewy body (alpha-synuclein) deposition in cerebral cortex neurons
What is the pathological difference between Lewy Body Dementia and Parkinson’s?
Lew bodies in:
Cerebral Cortex= Lewy body dementia
Substantial nigra= PD
What is the typical onset for the following 4 types of dementia?
1) Alzheimers
2) Vascular
3) Lewy body
4) Frontotemporal
Alzheimers: Gradual + progressive onset
Vascular: Abrupt (after stroke) or gradual (stepwise deterioration following multiple strokes)
Lewy body: Insidious onset + progressive with fluctuations
Frontotemporal: Insidious onset (50s/60s) then rapid progression
What is the clinical presentation for the following 4 types of dementia?
1) Alzheimers
2) Vascular
3) Lewy body
4) Frontotemporal
Alzheimer’s: memory, depression, language, visuospatial skills and behavioural signs
Vascular: focal neurological signs and vascular disease
Lewy body: visual hallucinations and Parkinsonism (tremors, falls and shuffling gait)
Frontotemporal: disinhibition, poor judgement, decreased motivation and socially inappropriate
What can be seen on a CT/MRI in Alzheimers Dementia?
Beta-amyloid plaques
Neurofibrillary tangles
Atrophy
Reduced cortical ACh
What may be seen on a CT/MRI in Frontotemporal Dementia?
Frontal/temporal atrophy
Picks cells
What may be seen on a CT/MRI in Vascular Dementia?
Blood vessels changes
Vascular infarcts
What may be seen on a CT/MRI in Lewy body Dementia?
Lewy bodies in cortex of midbrain
Generalised atrophy
List 5 tools used to assess cognition
- Addenbrookes cognitive examination-III (ACE-III)
- Montreal cognitive assessment (MoCA)
- Abbreviated mental test score (AMT)
- 6 item cognitive impairment test (6CIT)
- GP assessment of cognition (GPCOG)
What is the main investigative screening tool used for dementia?
ACE-III screening tool
What 5 cognitive domains does the ACE-III screening tool assess in dementia?
- Attention
- Memory
- Fluency
- Language
- Visiospatia
What MMSE scores supports dementia?
/30
≤24= dementia
21-25 = mild
0-20 = moderate
<10 = severe
What is the management of Alzheimers Dementia?
No cure
Acetylcholinesterase inhibitors e.g. Donepezil
NMDA antagonist e.g. Memantine
Treat depression and aggression/agitation
What is the management of Lewy body dementia?
No cure
Acetylcholinesterase inhibitors: e.g. donepezil
NMDA antagonist e.g. Memantine
RF reduction: e.g. high BP, high cholesterol, diabetes and smoking.
Levodopa
Physiotherapy
What is the management of vascular dementia?
No cure
Management of risk factors: e.g. high BP, high cholesterol, diabetes and smoking.
Acetylcholinesterase inhibitors: e.g. donepezil (only used in mixed dementia)
Improve/maintain cognitive function: structured group cognitive stimulation programmes, exercise, aromatherapy, therapeutic music/dancing and massage.
Aspirin
Advanced care planning
End of life care
What is the management of frontotemporal dementia?
No cure
Exercise, physiotherapy, speech and language therapy, and behaviour modification.
Serotonin reuptake inhibitors (SSRI): for behaviour (decreases disinhibition, anxiety, impulsivity and repetitive behaviours)
Atypical anti-psychotics: for agitation and behaviour
Where do you test sensation in the following dermatomes on the arm?
C5-T2
C5: Over deltoid
C6: Index finger
C7: Middle finger
C8: Little finger
T1: Inside arm
T2: Apex of axilla
Where do you test sensation in the following dermatomes on the leg?
L2-S2
L2: Anterior medial thigh
L3: Over knee
L4: Medial tibia
L5: Dorsum of foot running to big toe
S1: Lateral heel
S2: Popliteal fossa
Where do you test movement in the following myotomes on the arm?
C5-T1
C5: Shoulder abduction
C6: Elbow flexion
C7: Elbow extension
C8: Finger flexion
T1: Finger abduction
Where do you test movement in the following myotomes on the leg?
L2-S2
L2: Hip flexion
L3: Knee extension
L4: Ankle dorsiflexion
L5: Extension of big toe
S1: Ankle plantar flexion
S2: Knee flexion
What muscles does the radial nerve innervate?
Triceps and finger extensors
What muscles does the median nerve innervate?
LOAF:
Lateral 2 lumbricals
Oppenens brevis
Abductor pollicis brevis
Flexor pollicis brevis
What muscles does the ulnar nerve innervate?
Intrinsic muscles of the hand, lumbricals, hypothenar and interossei
What nerve is responsible for:
Finger flexion?
Finger extension?
Finger abduction?
Median
Radial
Ulnar
What is the most common winged scapula nerve lesion?
Long thoracic nerve (serratus anterior)
What nerve is responsible for the following movements?
Knee extension
Knee flexion
Ankle dorsiflexion
Big toe extension
Ankle plantar flexion
Knee extension: femoral L3
Knee flexion: sciatic/tibial L5, S1/2
Ankle dorsiflexion: peroneal L4
Big toe extension: peroneal L5
Ankle plantar flexion: tibial S1
Name some foot drop differentials?
Muscle: myopathy
Nerve: peroneal nerve, sciatic nerve
Root: L4/5
Anterior horn: MND
Brain: parasaggital mengingioma
Which lobe is Brocas area in and what is its function?
Frontal lobe of the dominant hemisphere (left)
Speech production
Which lobe is Wernicke’s area in and what is its function?
Temporal lobe (left) side of the brain
Speech comprehension
What is a subdural haemorrahage?
Vessel rupture below the dura mater
What is the most common cause of subdural haemorrhage?
Trauma
What is a extradural haemorrhage?
Bleeding above the dura mater
What can cause a extradural haemorrhage?
Serious head trauma: around the eye
What is a subarachnoid haemorrhage?
Berry cerebral aneurysms at points of bifurcation in the circle of Willis i.e ACA, PCA or MCA
What is the clinical presentation of brain haemorrhages?
Reduced GCS
Focal neurological symptoms: upgoing plantars, muscle weakness, hemiparesis and sensory problems
Headache (severe)
N&V
Seizures
Confusion
What spcifically indicates a extradural haemorrhage?
Pupil asymmetry (CN III compression)
What spcifically indicates a subdural haemorrhage?
Late signs/symptoms
What spcifically indicates a subarachnoid haemorrhage?
Sudden-onset Thunderclap headache
Occipital
How do extradural, subdural and epidural haematomas look on a non-contrast CT scan?
Extradural: biconvex
Subdural: crescent
Subarachnoid: hyperdense areas in subarach space
How are extradural haemorrhages managed?
Decompression: if required
Sit up in bed
Surgery: evacuation of blood + bleeding lesion ligation
What is the management of subdural haemorrhages?
Caniostomy
Craniotomy
Mannitol (reduces ICP)
What is the management of subarachnoid haemorrhages?
Nimodipine: CCB prevents vasospasms
Endovascular coiling
What is Multiple Sclerosis?
Autoimmune CNS demyelination via chronic inflammation
Peripheral nerves spared
20-40yr onset
What may be the first manifestation of MS?
Optic Neuritis (reduced visual acuity_
Describe 5 features of Optic Neuritis
1) Reduced visual acuity over days
2) Pain moving eyes
3) Exacerbated by heat/exercise
4) Afferent pupillary defect
5) Dyschromatopsia (especially red)
What is Lhermitte’s phenomenon?
Neck flexion → electric shock running down spine
What is Uhthoffs phenomenon?
Temperature increase worsens symptoms e.g. hot bath
What is the clinical presentation of MS?
Any neurological sign can be present in MS:
However NEVER involves LMN
Optic neuritis: loss of vision in one eye (CNII demyelination)
Diplopia: CNVI demyelination
Gaze paralysis: CNVI
Lhermitte’s phenomenon
Uhtoff’s phenomenon
Ataxia
Focal sensory symptoms: trigeminal neuralgia
Focal weakness: honers syndrome
How is MS diagnosed?
MRI: CNS lesions causing symptoms that:
- Last >24 hours
- Are disseminated in space (clinically or on MRI)
- Are disseminated in time (>1 month apart)
What is the management of Ms?
Acute?
Chronic?
No cure
Relapse/Acute:
Steroids (methylprednisolone may induce remission)
Chronic:
Disease-modifying drugs: maintain remission
- Beta-interferon: decreases inflammatory cytokine levels
- Monoclonal antibodies: alemtuzumab (anti-CD52) and natalizumab (anti-α4𝛃1-integrin).
Pain: gabapentin (anti epileptic)
Prevent relapse: Glatiramer
What are the 4 types of MS?
1) Clinically isolated syndrome (CIS)
2) Relapsing-remitting
3) Primary progressive
4) Secondary progressive
What is Clinically Isolated Syndrome MS?
First episode of demyelination (clinical presentation)
Not MS yet- does not fulfil space and time criteria!
MS diagnosis IF MRI shows lesions and ANOTHER attack occurs
What is Secondary Progressive MS?
Relapsing-remitting → progressive worsening of neurological functioning
What is Primary Progressive MS?
Symptoms worsen from onset
No relapses or remissions
What is Relapsing-Remitting MS?
Episodes (relapses) followed by recovery (remitting)
During remissions, there may be no symptoms or disease progression
What is the Glasgow Coma Scale?
Describes the level of consciousness in a person following a traumatic brain injury
How is the GCS scored?
1) Eye opening (E) 4
2) Verbal response (V) 5
3) Motor response (M) 6
The score may be expressed as e.g. ‘GCS 12 = E2 V4 M6’
Describe the GCS scoring
Motor response:
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None
Verbal response:
5. Orientated
4. Confused
3. Words
2. Sounds
1. None
Eye opening:
4. Spontaneous
3. To speech
2. To pain
1. None
What would the following GCS scores mean?
<8
3
15
<8= coma
3= min score
15= max score
What is giant cell arteritis?
Temporal arteritis
Vasculitis: immune-mediated inflammatory condition of the medium-large arteries
Typical Giant Cell Arteritis features?
Rare <50yrs
Severe unilateral headache around temple and forehead
Scalp pain when brushing hair: superficial temporal artery ischaemia
Jaw claudication: mandibular artery ischaemia
Blurred/diplopia
Irreversible painless complete sight loss can occur rapidly: opthalmic (retinal) artery ischaemia
Amaurosis fugax
How is GCA diagnosed?
CRP + ESR
FBC
Temporal artery US:
- Wall thickening
- Stenosis
- Occlusion
How is giant cell arteritis managed?
Corticosteroids (prednisolone): prevents irreversible visual loss
Aspirin
What is myasthenia gravis?
Acquired autoimmune condition
Affects postsynaptic NMJ
Abs against AChR in skeletal muscle
Results in weakness of the muscles
What are 7 clinical presentations of Myasthenia Gravis?
1) Symptoms better in the morning and worse throughout the day
2) Ptosis
2) Droopy mouth
3) Diplopia
4) Dysphagia
5) Dysarthria (facial muscles)
6) Muscle weakness
7) Dspnoea
What autoantibodies are involved in myasthenia gravis?
Acetylcholine receptor antibodies (AChR)
Muscle-specific tyrosine kinase (MuSK) antibodies
How is Myasthenia Gravis diagnosed?
Serum anti- acetylcholine (AchR) receptor
Serum anti- muscle specific Kinase (MuSK) antibodies
Thymomas (tumour)
Tensilon test: drug strengthens muscles so outstretched arms tire less easily
How is myasthenia gravis treated?
Pyridostigmine (reversible acetylcholinesterase inhibitor)
Corticosteroid (prednisolone)
What is Huntington’s disease?
Autosomal dominant
Degeneration of CNS neurons
How does Huntingtons occur?
Autosomal dominant:
1) Chr 4 produces Huntingtin protein
2) Mutation to chr 4 Huntington gene → CAG nucleotide repeats
3) Abnormal Huntingtin protein → neurodegenerative disorder
What condition is due to a CAG repeat?
Huntingtons
Signs of Huntingtons?
Asymptomatic until age 30-50
Progressive worsening of symptoms
Prodromal phase: cognitive, psychiatric or mood problems
Chorea
Eye movement disorders
Dysarthria
Dysphagia
Dementia
What is Progressive Supranuclear Palsy?
A Parkinson’s-plus syndrome
What is the clinical presentation of Progressive Supranuclear Palsy (PSP)?
Brain cell damage due to tau protein accumulation
What is the clinical presentation of Progressive Supranuclear Palsy?
- Falls and balance impairments
- Lack of interest, behaviour change, thought and memory impairment
- Hypertonia
- Dysarthria / Dysphagia
- Difficult eye and eyelid movements- focusing/ looking up/down
What is the most common cause of head tremor? (titubation)
Essential tremor
What may relieve an essential tremor?
What medication can be given?
Alcohol
Rest
Propanolol
What is motor neurone disease?
Upper and lower motor neurone degeneration in the CNS
What is the most common motor neuron disease?
Amyotropic lateral sclerosis (ALS)
What are the clinical features of motor neurone disease?
Starts up, then goes down
MND does NOT affect eye movement (differentiate from myesthenia gravis)
Signs ofLMN disease: everything goes down
Reduced tone
Reduced reflexes
Fasciculations
Muscle wasting
Signs ofUMN disease: everything goes up
Increased tone/spasticity
Brisk reflexes
Upgoing plantar responses
NO SENSORY SIGNS
Sphincters unaffected
How is a Hoffmans sign elicited?
Flick the middle finger nail:
Flexion of ipsilateral thumb or index = positive sign = UMN pathology
Give 4 signs of UMN weakness
- Increased muscle tone
- Hyperreflexia
- Spasticity
- Minimal muscle atrophy
Give 5 signs of LMN weakness
- Decreased muscle tone
- Hyporeflexia
- Flaccid
- Muscle atrophy
- Fasciculations
What is the management of ALS?
Riluzole
Baclofen
Which type of MND has the worst prognosis?
Progressive bulbar palsy: difficulty swallowing / speech / respiratory insufficiency
What are red flags for headaches?
1) Thunderclap: ‘worst headache I’ve ever had’.
2) Worse in the morning
2) Sudden + severe
2) Age >50
3) Neck pain/stiffness, photophobia
4) Fever
5) Papilloedema
6) New onset neuro deficit
7) Vomiting
8) Dizziness and visual disturbances/atypical aura (over an hour)
What is Giant Cell Arteritis?
Temporal arteritis
Vasculitis: immune-mediated inflammatory condition of the medium-large arteries
Who does GCA tend to affect?
Females >males
Scandinavians
>50 yrs
What is the clinical presentation of Giant Cell Arteritis?
Myalgia
Fever
Unilateral Headache
Scalp pain when brushing hair: superficial temporal artery ischaemia
Jaw claudication: mandibular artery ischaemia
Diplopia
Irreversible painless complete sight loss can occur rapidly: opthalmic(retinal) artery ischaemia
Amaurosis fugax
What Anaemia is seen in Giant Cell Arteritis?
Normocytic Normochromic
How is Giant Cell Arteritis investigated?
Increased ESR
Increased LFTs (ALP)
Increased IgGs and complements
(CK not elevated as no muscle damage)
Temporal artery US:
- Wall thickening
- Stenosis
- Occlusion
Temporal artery biopsy: confirms
What is the management of Giant Cell Arteritis?
Corticosteroids (prednisolone): prevents irreversible visual loss
Aspirin
What is the main complication of Giant Cell Arteritis?
BLINDNESS
What is the difference between a facial palsy caused by an upper or lower motor neurone lesion?
Upper motor neurone lesion spares the upper head e.g ‘wrinkle forehead/raise eyebrows’
What is Bells Palsy?
What is the classic triad?
Lower motor neurone palsy of the facial nerve (7th)
Causes:
1) Facial droop on one side of the face
2) Flat wrinkles on one side of forehead
3) Can’t close one eyelid
At what age are you more likely to get Myasthenia Gravis?
Women: <40
Men: >60
What muscles are weakened in Myasthenia Gravis?
Weakness of extra-ocular muscles causing:
1) Diplopia
2) Ptosis (droopy eyelid)
What is a Myasthenic Crisis?
Weakness of breathing muscle = life threatening
What type of hypersensitivity reaction is Myasthenia Gravis and Multiple Sclerosis?
MG: type II (antibody mediated- AChR/MuSK)
MS: type IV (cell-mediated- T cells)
What is Charcots Neurological Triad?
1) Dysarthria (dysfunctional eating, talking and swallowing)
2) Intention tremor (muscle weakness, spasms, ataxia and paralysis)
3) Nystagmus (optic neuritis, greying of vision, pain and diplopia)
Linked to MS
What visual defects are caused within the Optic Chiasm?
Bitemporal hemianopia
What is Cauda Equina?
Sudden spinal stenosis at L2/L3
Give 5 signs of Cauda Equina
- Bilateral sciatic: pain radiates down leg to foot
- Saddle anaesthesia
- Bladder/bowel dysfunction
- Erectile dysfunction
- Leg weakness
What is polypharmacy?
A large number of unnecessary medications (4+)
How often should a patient be repositioned to prevent pressure sores?
Normal risk: every 6 hrs
High risk: every 4hrs
Give 3 treatment options for malnutrition
- Encouraging food and drink intake
- ONS: yoghurts, milkshakes, juices etc
- Enteral feeding
- Parenteral feeding
Define refeeding syndrome
Electrolyte imbalance from reintroducing food after starvation (>10 days)
What is the clinical presentation of Re-feeding syndrome?
Drop in phosphate due to rapid initiation of food →:
▪ Rhabdomyolysis
▪ Respiratory/cardiac failure
▪ Hypotension
▪ Arrhythmias
▪ Seizures
What is the management of re-feeding syndrome?
Slow refeeding
Thiamine
Monitor :
- Hypophosphatemia
- Hypokalaemia
- Hyperglycaemia
- Hypermagnesemia
Define frailty
A state of increased vulnerability resulting from an ageing associated decline in reserve and function across multiple physiologic systems.
The ability to cope with everyday stressors is compromised.
