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Neurology conditions Flashcards

1
Q

What is Bell’s palsy?

A

Acute unilateral peripheral facial nerve palsy, physical exam and history unremarkable.
Fully evolves within 72 hours

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2
Q

What are the LMN causes of Bell’s palsy?

A 
Idiopathic
Pregnancy
Diabetes Mellitus
Iatrogenic
Infective (Herpes)
Ramsay hunt syndrome (Herpes zoster)
Trauma
Neurological
Neoplastic
Hypertension 
Sarcoidosis 
Sjorgen's
Melkersson-Rosenthal syndrome
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3
Q

What are the causes of UMN Bell’s palsy?

A

Cerebrovascular disease
Intracranial tumours
Multiple slcerosis
Syphillis
HIV
Vasculitides
IF B/L immunosuppression, GBS or lyme disease
Recurrent: Lymphoma, sarcoidosis, lyme disease
Children - Lyme disease and middle ear disease

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4
Q

How can you tell the difference between LMN or UMN causes of Bell’s palsy?

A

A UMN bell’s palsy is forehead-sparing

Can still lift their eyebrows

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5
Q

What are the risk factors for Bell’s palsy?

A 
Intracranial influenza vaccinaiton
Pregnancy
Upper respiratory tract infection
Black or Hispanic ancestry
Arid/cold climate
Hypertension
Family history of Bell's palsy
Diabetes
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6
Q

What are the symptoms for Bell’s palsy?

A 
Onset and progression of palsy
Presence of fever
Prior episodes of facial palsy
Otological symptoms
Presence of other cranial neuropathies
Collagen vascular
Use of neurotoxic medicaitons
Known, prior or current malignancy
Pregnancy
Immunosuppression
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7
Q

What are the signs of Bell’s palsy?

A

Head and neck examination
Cranial nerve exam
Eyebrow sparing

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8
Q

What investigations are done for Bell’s palsy?

A

Serology (Lyme, Herpes and zoster)

Check BP in children

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9
Q

Why do you check BP in children with Bell’s palsy?

A

Children present with facial palsy in Aortic coarctation

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10
Q

What is the management for Bell’s palsy?

A

Steroids (prednisolone to people >16 within 72 hours)
Antivirals (moderate benefit)
Surgery (if no reduced paralysis)

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11
Q

What are the complications for Bell’s palsy?

A

Keratoconjunctiva sicca
Ectropion (Sagging eyelid)
Contracture and synkinesis
Gustatory hyperlacrimation

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12
Q

What are CNS tumours?

A

Tumours of the CNS

Cannot truly differentiate into benign and malignant as cause severe damage either way

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13
Q

How do you differentiate CNS tumours?

A

High-grade
Low-grade
Metastases

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14
Q

What makes a high-grade tumour?

A

Glioma and glioblastoma multiforme
Primary central lymphoma
Medulloblastoma

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15
Q

What is a low-grade tumour?

A 
Meningioma
Acoustic neuroma
Neurofibroma
Pituitary tumour
Craniopharyngioma
Pineal tumour
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16
Q

What cancers cause brain metastases?

A 
Lung
Breast
Stomach 
Prostate
Thyroid
Colorectal
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17
Q

What causes CNS tumours?

A

Arise from any cells in the CNS

e.g. glial cells, ependymal cells, oligodendrocytes

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18
Q

What are the risk factors for CNS tumours?

A

Ionising radiation
Immunosuppression (e.g. HIV)
Inherited syndromes (e.g. Neurofibromatosis, tuberous sclerosis)

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19
Q

What are the signs and symptoms of CNS tumours?

A 
Depends on size and location of tumour
Headache (Worse in morning and laying down)
Nausea and vomiting
Seizures
Progressive focal neurological deficits
Cognitive and behavioural symptoms 
Papilloedema
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20
Q

What clinical features localise a tumour to the temporal lobe?

A

Dysphasia
Contralateral homonymous hemianopia
Amnesia
Odd/inexplicable phenomena

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21
Q

Which clinical features localise a tumour to the frontal lobe?

A 
Hemiparesis
Personality change
Broca's dysphasia
Unilateral anosmia
Concrete thinking
Executive dysfunction
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22
Q

What clinical features localise a tumour to the parietal lobe?

A

Hemisensory loss
Reduced 2 point discrimination
sensory inattention
Dysphasia

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23
Q

What clinical features localise a tumour to the occipital lobe?

A

Contralateral visual field defects

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24
Q

What are the investigations for CNS tumours?

A

CRP/ESR (eliminate causes)
CT/MRI/PET (visualise tumour)
MRI angiography (see blood supply to tumour)
Biopsy/Tumour removal

Distant mets are rare with primary CNS tumours

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25
Q

What are cluster headaches?

A

Neurological disorder characterised by recurrent, severe headaches on one side of the head typically around the eye, tending to recur over a period of weeks

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26
Q

What are the 2 types of cluster headaches?

A

Episodic

Chronic

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27
Q

What are episodic cluster headaches?

A

Occur in periods lasting 7 days - 1 year

Separated by pain-free periods lasting a month or longer

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28
Q

What are chronic cluster headaches?

A

Occurring for 1 year without remission or with short-lived remissions of less than a month.
Can arise de novo or from episodic cluster headaches

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29
Q

What causes cluster headaches?

A

Unknown
May be surperficial temporal artery smooth muscle hyperreactivity to 5HT
Genetic factor implicated (Autosomal Dominant gene has a role)

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30
Q

What are the risk factors for cluster headaches?

A 
Male
Family history
Head injury
Smoking
Drinking
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31
Q

What are the signs and symptoms of cluster headaches?

A

Occur in clusters lasting 4-12 weeks

Occur at night, 1-2hrs after sleeping`

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32
Q

What are the symptoms of cluster headaches?

A 
Occurs rapidly around 10 mins
Intense, sharp and penetrating pain
Centred around eye, temple or forehead
Unilateral affects same side
Lasts 30-45 mins
Find it difficult to stay still and will pace around and bang their heads on things
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33
Q

What are the associated symptoms of cluster headaches?

A

Ipsilateral features:

  • Ipsilateral lacrimation
  • Rhinorrhoea
  • Nasal congestion
  • Eye lid swelling
  • Facial swelling and flushing
  • Conjunctival infection
  • Partial Horner’s syndrome
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34
Q

What triggers cluster headaches?

A

Alcohol
Exercise and solvents
Sleep disruption

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35
Q

What are the investigations of cluster headaches?

A

Clinical diagnosis based on history

Neurological examination may be useful

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36
Q

What is Epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures (paroxysmal synchronised cortical electrical discharges)

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37
Q

What are the types of seizures?

A 
Partial
- Complex
- Simple
Generalised
- Tonic-clonic
- Abscence
- Myoclonic
- Atonic
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38
Q

What are the structural causes of epilepsy?

A 
Cortical scarring
Developmental
Space-occupying lesion
Stroke
Hippocampal sclerosis
Vascular malformations
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39
Q

What are the non-epileptic causes of seizures?

A 
Trauma
Stroke
Haemorrhage
Raised ICP
Alcohol or Benzodiazepin withdrawal
Liver disease 
Infection
High temperature
Drugs (Cocaine, tramadol, theophylline, tricyclics)
Metabolic disturbance
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40
Q

What are the ‘other’ causes of epilepsy?

A

Tuberculous sclerosis
Sarcoidosis
SLE
PAN

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41
Q

What are common things that look like seizures?

A

Syncope
Migraine
Non-epileptiform seizure disorder (e.g. dissociated disorder)

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42
Q

What are the types of frontal/partial seizure epilepsy?

A

Frontal lobe focal motor seizure
Temporal lobe seizure
Frontal lobe complex partial seizure

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43
Q

What are the signs and symptoms of frontal lobe focal motor seizure?

A

Motor convulsions
Jacksonian march
Post-ictal flaccid weakness (Todd’s paralysis)

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44
Q

What is a jacksonian march?

A

Muscular spasm spreads from distal limb to ipsilateral face

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45
Q

What are the signs and symptoms of temporal lobe seizure?

A

Aura (Visceral or psychic symptoms)

Hallucinations (Usually olfactory or affecting taste)

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46
Q

What are the signs and symptoms of frontal lobe complex partial seizure?

A

Loss of consciousness
Involuntary actions/disinhbition
Rapid recovery

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47
Q

What are the types of generalised seizures?

A

Tonic-clonic (Grand mal)
Abscence (Petit mal)
Non convulsive status epilepticus

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48
Q

What are the signs and symptoms of grand mal seizures?

A

Vague symptoms before attack (irritability)
Tonic phase (generalised muscle spasm)
Clonic phase (Repetitive synchronous jerks)
Faecal/urinary incontinence
Tongue bitings
Post-ictal phase: Impaired consciousness, lethargy, confusion, headache, back pain, stiffness

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49
Q

What are the signs and symptoms of petit mal seizures?

A

Onset in childhood
Loss of consciousness but maintained postures
The patient will appear to stop talking and stare
NO post-ictal phase

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50
Q

What are the signs and symptoms of non-convulsive status epilepticus?

A

Acute confusional state
Often fluctuating
Difficult to distinguish from dementia

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51
Q

What are the investigations for Epilepsy?

A 
FBC
U&E
LFTs
Glucose
Calcium
Magnesium
ABG
Toxicology screen
Prolactin
EEG
CT/MRI
Other
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52
Q

How do you manage newly diagnosed epilepsy?

A

Start anti-convulsant treatment after >2 unprovoked seizures
Drugs change depending on type of epilepsy
- Generalised: Sodium valproate or Lamotrigine
- Abscence: Sodium valproate, lamotrigine or ethosuximide
- Partial: Carbamezapine

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53
Q

What is status epilepticus?

A

A seizure lasting >30 mins or repeated seizures without recovery and regain of consciousness in between

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54
Q

How do you manage status epilepticus?

A 
ABC approach
Check glucose
IV lorazepam or IV/PR Diazepam
If they recur, use IV phenytoin - need ECG monitor
If fails consider general anaesthesia
Treat cause
Check plasma levels of anticonvulsants
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55
Q

What are the complications of epilepsy?

A 
Fractures from tonic-clonic seizures
Behavioural problems
Sudden death
Complications of drugs:
- Gingival hypertrophy (Phenytoin)
- Neutropenia and osteoporosis (Carbamezapine)
- Stevens-Johnson syndrome (Lamotrigine)
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56
Q

What is an extradural haemorrhage?

A

Bleeding and accumulation of blood in the extradural space -between dura mater and skull

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57
Q

What causes an extradural haemorrhage?

A

Trauma

- Usually due to fracture of the pterion area - rupturing the middle meningeal artery.

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58
Q

What are the risk factors for extradural haemorrhage?

A

Age
Bleeding tednency (E.g. haemophilia)
Drugs (warfarin)

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59
Q

What are the symptoms of extradural haemorrhage?

A

Temporary loss of consciousness /drowsiness
Then Lucid interval (resolved consciousness levels)
Then progressive deterioration in GCS as ICP rises
Increasing severe headache/vomiting/confusion/ fits +/- hemiparesis with brisk reflexes and upgoing plantars
Ipsilateral pupil dilation, coma deepens, b/l limb weakness

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60
Q

What are the signs of extradural haemorrhage?

A 
Scalp traumas or fracture
Signs of raised ICP (dilated, unresponsive pupils)
Cushing's response 
- Hypertension
- Bradycardia
- Irregular breathing
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61
Q

What are the investigations for extradural haemorrhage?

A

Urgent CT scan

  • Check for haematoma, may get a contracoup injury on opposite side
  • Look for features of raised ICP e.g. midline shift
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62
Q

What is Guillain-Barre syndrome?

A

GBS is a type of acute inflammatory neuropathy.
Clinically defined syndrome associated with motor difficulty, absence of deep tendon reflexes, paraesthesias without sensory losses and an increase in CSF albumin without cellular reaction

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63
Q

What are the subtypes of GBS?

A

Acute inflammatory demyelinating polyardiculoneuropathy
Acute motor and sensroy axonal neuropathy
Acute motor axonal neuropathy
Acute sensory neuropathy
Acute pandysautomnia

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64
Q

Which Antibodies are the types of GBS associated with?

A

AIDP - none
AMSAN - GM1, GM1b & GD1a
AMAN - GM1, GM1b, GD1a, GalNac-GD1a
Acute sensory neuropathy - GD1b

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65
Q

What are the risk factors for GBS?

A

History of GI or respiratory infections (1-3 weeks after)
Association with zika virus
Vaccinaitons
Malignancies (lymphomas)
Pregnancy (Decreases during pregnancy and increases after delivery)

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66
Q

What are the symptoms of GBS?

A 
Weakness
Pain
Reflexes
Sensory symptoms
Autonomic symptoms
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67
Q

What are the signs of GBS?

A 
Hypotonia
Demonstrate altered sensation or numbness
Reduced or absent refelxes
Fasciculation may occasionally be absent
Facial weakness (asymmetrical)
Autonomic dysfunction
Respiratory muscle paralysis
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68
Q

What investigations are done for GBS?

A 
Electrolytes
Lumbar puncture (Raised CSF protein, no raised CSF cells, not until weakness)
Antibody screen
Spirometry
Nerve conduction studies
ECG
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69
Q

What is the management of GBS?

A 
Plasma exchange
IV immunoglobulin
DVT prophylaxis
Admission to ICU
Pain relief
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70
Q

What are the complications of GBS?

A

Persistent paralysis
Respiratory failure requiring ventilation
Hypotension or Hypertension
Thromboembolism, pneumonia, skin breakdown
Cardiac arrhythmia
Ileus
Aspiration pneumonia
Urinary retention
Psychiatric problems e.g. depression, anxiety

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71
Q

What is Horner’s syndrome?

A

Disruption of sympathetic nerves supplying the eye

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72
Q

What are the three things of Horner’s syndrome?

A 
Partial ptosis (upper eyelid drooping)
Miosis (Pupillary constriction leading to anisocoria)
Hemifacial anhidrosis (abscence of sweating)
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73
Q

What causes horner’s syndrome?

A

Cranial nerve lesions
Preganglionic nerve lesions
Postganglionic nerve lesions

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74
Q

What causes cranial nerve lesions?

A 
MS 
Cerebrovascular accidents
Pituitary or basal skull tumours
Basal meningitis
Neck trauma
Syringiomyelia
Anrold-chiari malformation
Spinal cord tumours
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75
Q

What causes pre-ganglionic nerve lesions?

A 
Apical lung tumours (Pancoast tumour)
Lympadenopathy
Lower brachial plexus trauma or rib
Aortic aneurysm
Trauma or surgical injury
Neuroblastoma
Mandibular dental abscess
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76
Q

What causes post-ganglionic nerve lesions?

A 
Cluster headaches or migraines
Herpes zoster infectoin
Internal carotid artery dissection
Raeder's syndrome
Carotid-cavernous fistula
Temporal arteritis
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77
Q

What investigations should be done in Horner’s syndrome?

A

CXR
CT/MRI
CT angiography/Carotid ultrasound

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78
Q

What is the pharmacological testing for Horner’s?

A
  • Cocaine eye drops normally cause dilatation of eyes but wont in horners
  • Apraclonidine is an alternative to cocaine - dilates a horner’s pupil but not a normal one
  • Hydroxyamfetamine causes dilatation in first and second order lesions but not third
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79
Q

What is the management of horner’s

A

Treat underlying cause

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80
Q

What is Huntington’s disease?

A

Autosomal dominant trinucleotide repeat disease (CAG repeat on chromosome 4)

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81
Q

What characterises huntington’s disease?

A

Progressive chorea and dementia

Typically starts in middle age

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82
Q

What causes huntington’s disease?

A

The huntingtin gene codes for huntingtin
In the huntingtin gene there is a trinucleotide repeat expansion that results in toxic gain of function
Causes atrophy and neuronal loss of striatum and cortex
Autosomal dominant
Earlier age of onset with each generation

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83
Q

What are the symptoms of huntington’s disease?

A 
Family history
Insidious onset in middle age
Progressive
Early symptoms
Late symptoms
Drug history (cocaine, antipsychotics)
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84
Q

What are the early symptoms of huntington’s disease?

A 
Lability
Dysphoria
Irritability
Incoordination
Fidgeting
Clumsiness
Mental inflexibility
Anxiety
Develops in dementia
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85
Q

What are the late symptoms of huntington’s disease?

A 
Rigid
Involuntary, jerky, duskinetic movement soften accompanied by grunting and dysarthria (chorea)
Dementia
Fits
Akinetic
Bed-bound
Death
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86
Q

What are the signs of huntington’s disease?

A 
Chorea
Dysarthria
Slow voluntary sacades
Supranuclear gaze restriction
Parkinsonism
Dystonia
MMSE shows cognitive and emotional deficits
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87
Q

What are the investigations for huntington’s disease?

A

Genetic analysis
- Diagnosed if >39 CAG repeats
- Reduced penetrance leads to intermediate number of CAG repeats
Imaging
- Brain MRI/CT show symmetrical atrophy of striatum and butterfly dilation of the lateral ventricles
Bloods

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88
Q

What is Hydrocephalus?

A

Enlargement of the cerebral ventricular system due to accumulation of CSF.
Too much CSF produced, blocked CSF flow or insufficient CSF reabsorbing

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89
Q

What are the types of CSF?

A

Non-obstructive / communicating
Hydrocephalus ex vacuo
Obstructive / non-communicating hydrocephalus

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90
Q

What is a communicating hydrocephalus?

A

Impaired CSF reabsorption into the subarachnoid villi

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91
Q

What is a hydrocephalus ex vacuo?

A

Apparent enlargement of the ventricles as a compensatory change due to brain supply

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92
Q

What is a non-communicating hydrocephalus?

A

Blockage of CSF within the ventricles

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93
Q

What are risk factors for hydrocephalus?

A 
Congenital:
- Premature birth causing bleeding in ventricles
- Uterus infection
- CNS abnormal development
Acquired:
- CNS infeciton
- Bleeding in brain from trauma/stroke
- Age >65 years
- Vascular disease
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94
Q

What are the symptoms of obstructive/communicating hydrocephalus?

A

Acute drop in GCS

6th nerve palsy causing diplopia

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95
Q

What are the symptoms of normal pressure hydrocephalus?

A

Dementia
Gait disturbance
Urinary incontinence

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96
Q

What are the signs of obstructive hydrocephalus?

A

Low GCS
Papilloedema
6th nerve palsy

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97
Q

Why is the 6th cranial nerve most susceptible to raised ICP?

A

It has the largest intracranial path

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98
Q

What are the signs of obstructive jaundice in neonates?

A 
Increased head circumference
Sunset sign (downward cojugate deviation of the eyes)
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99
Q

What investigations are done for Hydrocephalus?

A

CT head (First line)
CSF
- Ventricular drain or LP, indicate pathology
LP (Contraindicated in raised ICP, therapeutic in normal pressure hydrocephalus)

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100
Q

What is a migraine?

A

Chronic, episodic, neurological disorder that presents in early-to-mid life

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101
Q

What causes migraines?

A

Brains are hyperexcitable to a variety of stimuli

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102
Q

What are the risk factors for migraines?

A 
Family history of migraine
High caffeine intake 
Exposure to barometric pressure
Female sex
Obesity
Habitual snoring
Stressful life events
Overuse of headache movements
Lack of sleep
Low socio-economic status
Allergies or asthma
Hypertension
Hypothyroidism
Diet
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103
Q

What are the symptoms for migraine?

A

Visual or other aura
Aura without headache
Episodic severe headaches without aura, often premenstrual, U/L, with allodynia

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104
Q

What are the signs for migraine?

A

None

105
Q

What are the criteria for migraines without aura?

A 
>/=5 headaches lasting 4-72 hours
Nausea / vomiting
Photo/phonophobia
With 2 of:
- Unilateral 
- Pulsating
- Abnormalities suggesting another cause
106
Q

What are the investigations for Migraines?

A 
ESR
LP
CSF culture
CT head
MRI brain
107
Q

What are red flags seen on examination for migraines?

A

Papilloedema
New seizure
Abnormal neurological signs
New-onset cluster headaches

108
Q

What are the orange flags seen on examination for migraines?

A

New headache and no other clear diagnosis
Headache aggravated by exertion or valsalva
Headache with vomiting
New headache in 50+
Changed pattern of headaches

109
Q

What are the yellow flags for migraines?

A

Migraine

Memory loss

110
Q

What is the management for migraines?

A

Relieve symptoms (NSAIDs > Triptans) - if not, paracetamol
Anti-emetics for N&V
High flow O2 via non-rebreather mask
Reduce frequency and severity of migraine attacks
Identify trigger factors to avoid them
Prophylaxis if occurs >2/month

111
Q

What can be done as prophylaxis for migraines?

A

Start low-dose and re-evaluate after trial
Non-pharmaceutical help: CBT, Biofeedback- assisted relaxation
Treat for 4-6 months
Menstrual migraine > hormonal therapy to suppress menses
Main drugs: Anticonvulsants (topiramate), tCAs and Beta blockers
CCBs for hemiplegic migraine and migraine with brainstem aura

112
Q

What are the complications for migraines?

A 
Status migrainosus
Migrainous infarction
Migraine-triggered seizures
Depression
Chronic migraine
Persistent aura without infarciton
113
Q

What is motor neuron disease?

A

A progressive neurodegenrative disorder of cortial, brainstem and spinal motor neurons (LMN and UMN) - this is selective loss of neurons in more cortex, cranial nerve nuclei and anterior horn cells!
- No sesnory loss

114
Q

What are the subtypes of MND?

A

Amyotrophic lateral sclerosis (ALS)
Progressive muscular atrophy variant
Progressive bulbar palsy variant
Primary lateral sclerosis variant

115
Q

What is ALS?

A

Lou gherig’s disease

Combined degeneration of upper and lower motor neruoens resulting in a mix of LMN and UMN signs

116
Q

What is progressive muscular atrophy variant MND?

A

Only LMN signs

Better prognosis

117
Q

What is progressive bulbar palsy variant MND?

A 
Only affects CN IX-XII
Dysarthria
Dysphagia
Wasted fasciculating tongue
Brisk jaw jerk reflex
118
Q

What is primary lateral sclerosis variant MND?

A 
Loss of Betz cells in motor cortex
UMN pattern of weakness
Brisk reflexes
Extensor plantar responses
No LMN signs
119
Q

What causes motor neuron disease?

A

Unknown
Free radical damage and gluatamate excitotoxicity have been implicated
Associated with frontotemporal lobar dementia

120
Q

What are the risk factors for MND?

A

Genetic predisposition/family history
Age > 40
Smoking
Athleticism/ family history

121
Q

What are the symptoms of MND?

A

Weakness of limbs (proximal myopathy)
Speech disturbance
Swallowing disturbances (choking on food)
Behavioural changes

122
Q

What are the signs of MND?

A 
Combo of UMN and LMN signs
LMN
- Muscle wasting
- Fasciculations 
- Flaccid weakness
- Hyporeflexia
UMN
- Spastic weakness
- Extensory plantar response
- Hyperreflexia
Sensory exam is normal
Frontotemporal dementia occurs in 25%
123
Q

What are the investigations for MND?

A

Clinical diagnosis
EMG: Diffused/ongoing/chronic denervation seen
Nerve-conduction studies
MRI to exclude cord compression/brainstem lesions
Bloods
- Mild elevation of CK
- ESR (Raised)
- Anti GM1-ganglioside antiboides (Negative)

124
Q

What is multiple sclerosis?

A

Inflammatory demyelinating disease of the CNS - discrete plaques of demyelination occur at multiple CNS sites, from T-cell mediated immune response

125
Q

What are the types of MS?

A

Relapsing-remitting MS
Clinically isolated syndrome
Primary progressive MS
Marburg variant

126
Q

What is relapsing-remitting MS?

A

Commonest form

Clinical attacks of demyelination with poor healing in between attacks

127
Q

What is Clinically isolated syndrome?

A

Single clinical attack of demyelination
The attack itself doesn’t count as MS
10-50% progress to MS

128
Q

What is Primary progressive MS?

A

Steady accumulation of disability with NO relapsing-remitting MS

129
Q

What is Marburg variant MS?

A

Severe fulminant variant of MS leading to advanced disability or death within weeks

130
Q

What causes MS?

A

Unknown
AI bases with potential environmental trigger in genetically susceptible individuals
Immune-mediated damage to myelin sheaths results in impaired axonal conduction

131
Q

What are the risk factors of MS?

A

EBV exposure

Prenatal vitamin D levels

132
Q

What are the symptoms of MS?

A 
Varies on site
Usually monosymptomatic
Optic neuritis (most common)
Sensory 
Motor 
Autonomic
Psychological/cognitive
Sexual
GI
Cerebellum
Early on, relapses then remits to full recovery
Uhthoff's sign
Lhermitte's sign
133
Q

What are the optic neuritis symptoms?

A

Unilateral deterioration of visual acuity and colour perception
Pain on eye movement
Rapid loss of centrla vision

134
Q

What are the sensory symptoms of MS?

A

Pins and needles
Numbness
Burning

135
Q

What are the motor symptoms of MS?

A

Limb weakness
Spasms
Stiffness
Heaviness

136
Q

What are the autonomic symptoms of MS?

A

Urinary urgency
Hesitancy
Incontinence
Impotence

137
Q

What are the psychological/cognitive symptoms of MS?

A

Depression
Psychosis
Amnesia
Reduced executive fucntioning

138
Q

What are the sexual symptoms of MS?

A

Erectile dysfunction

Anorgasmia

139
Q

What are the GI symptoms of MS?

A

Swallowing disorders

Constipation

140
Q

What are the cerebellar symptoms of MS?

A

Trunk and limb ataxia
Intention tremor
Scanning speech falls

141
Q

What is Uhthoff’s sign?

A

Worsening of neurological symptoms as body gets overheated from hot weather, saunas, hot tubs etc

142
Q

What is Lhermitte’s sign?

A

Electrical sensation that runs down the back and into the limbs when neck is flexed

143
Q

What are the signs of MS?

A 
Optic neuritis
Visual field testing
RAPD
Internuclear ophthalmoplegia
Paraesthesia
UMN signs
Limb ataxia
Dysdiadochokinesia
Ataxic wide-based gait
Scanning speech
Central scotoma
Loss of coloured visions
Impaired visual acuity
144
Q

What are the investigations for MS?

A

Diagnosis based on finding of 2 or more CNS lesions with corresponding symptoms, seperated in time and space - Mcdonald criteria!
Lumbar puncture
- Microscopy (exclude infection/inflammatory causes)
- CSF electrophoresis shows unmatched oligoclonal bands
MRI brain
- Plaques identifies
- Gadolinium enhancement shows active lesions
Evoked potentials
- Visual, auditory and somatosensory evoked potentials may show delayed conduction velocity

145
Q

What is Myasthenia gravis?

A

An AI disease affecting the neuromuscular junction producing weakness in skeletal muscles

146
Q

What causes myasthenia gravis?

A

Antibodies against the nicotininc acetylcholine receptor which interferes with the neuromuscular transmission via depletion os post-synaptic receptor sites
Can be paraneoplastic

147
Q

What is Lambert-Eaton syndrome?

A

Paraneoplastic subtype of MG caused by auto antibodies against pre-synaptic calcium channels, leading to impairment of acetylcholine release

148
Q

What are the risk factors for MG?

A

AI conditions

149
Q

What are the symptoms of MG?

A 
Muscle weakness that worsens with repetitive use or towards the end of the day - fatiguability
Ocular symptoms
- Drooping eyelids
- Diplopia
Bulbar symptoms
- Facial weakness (myasthenic snarl)
- Disturbed hypernasal speech
- Difficulty smiling, chewing or swallowing
150
Q

What is the order of muscles that become weakened?

A

Extraocular > Bulbar > Face > Neck > Limb girdle > Trunk

In lambert-eaton syndrome fatiguability improves with use

151
Q

What are the signs of MG?

A 
May be generalised
May be bulbar (relating to medulla oblongatea)
May be ocular
Eye signs
- Ptosis
- complex opthalmoplegia
- ocular fatigue
Ice on eyes test (putting ice packs on eyelids for 2 mins improves transmission and reduces ptosis)
Bulbar signs (reading aloud causes dysarthria or nasal speech)
Limbs 
- Test power 
- tendon reflexes are normal
152
Q

What are the investigations for MG?

A 
CK (Exclude myopathies)
Serum acetylcholine receptor antibody 
If seronegative 
- TFTs
- Anti-voltage gated calcium channel antibodye
Tensilon test (Not used)
Nerve conduction study 
EMG
CT thorax/CXR
- visualise thymoma or lung malignancies
153
Q

What is Neurofibromatosis?

A

An Autosomal dominant genetic disorder affecting cells of neural crest origin, resulting in the development of multiple neuroctaneous tumours
There are 2 types

154
Q

What is type 1 neurofibromatosis?

A

Von Recklinghausen’s disease

  • Peripheral and spinal neurofibromatosis
  • Multiple cafe au lait spots
  • Freckling (axillary/inguinal)
  • Optic nerve glioma
  • Lisch nodules (on iris)
  • Skeletal deformities
  • Phaeochromocytomas
  • Renal artery stenosis
155
Q

What is Neurofibromatosis type 2?

A

A condition characterised by:

  • Schwannomas
  • Meningiomas
  • Gliomas
  • Cataracts
156
Q

What causes neurofibromatosis?

A

Associated with mutations in tumour suprression genes NF1 and NF2

157
Q

What are the risk factors for neurofibromatosis?

A

Severe crush trauma

Parent with neurofibromatosis

158
Q

What are the symptoms of type 1 neurofibromatosis?

A 
Family history
Skin lesions
Learning difficulties (40%)
Headaches
Disturbed vision (optic gliomas)
Precoccious puberty (lesions of pit. gland from an optic glioma)
159
Q

What are the symptoms of type 2 neurofibromatosis?

A 
Family history
Hearing loss
Tinnitus
Balance problems
Headache
Facial pain
Facial numbness
160
Q

What are the signs of type 1 neurofibromatosis?

A

5+ cafe au lait macules of >5mm (prepubertal)
5+ cafe au lait macuels of >15mm (Post-pubertal)
Freckling in armpit or groin
Lisch nodules (hamartomas on the iris - slit lamp)
Spinal scoliosis
Short stature

161
Q

What are the signs of type 2 neurofibromatosis?

A

Few or no skin lesions

Sensorineural deafness with facial nerve palsy or cerebellar signs (if schwannoma is large)

162
Q

What are the investigations for neurofibromatosis?

A 
Full body exam for skin lesions
Ophthalmological assessment
Audiometry
MRI brain and spinal cord
Skull X-ray (sphenoid dysplasia in NF1)
Genetic testing
163
Q

What is Parkinsons’s disease?

A

A neurodegenerative disorder

164
Q

What is the triad of parkinsonism?

A

Tremor
Rigidity/increased tone
Bradykinesia/hypokinesia

165
Q

What causes primary parkinson’s disease?

A

Genetic component, subsequent environmental factors/exposure contributing to evolution of clinical disease

166
Q

What causes secondary parkinson’s disease?

A

Neuroleptic therapy (e.g. schizophrenia)
Vascular insults (e.g. in basal ganglia)
MPTP toxin from illicit drug contamination
Post-encephalitis
Repeated head injury
Manganese of copper toxicity (wilson’s diseae)
HIV

167
Q

What are the risk factors for parkinson’s disease?

A

Increasing age
History of familial PD in younger-onset disease
Mutation in gene encoding glucocerebrosidase
Metal exposure
Male
Head truama
Toxin exposure
Occupation (Teacher, HCP, construction worker, carpenter or cleaner)

168
Q

What are the key diagnostic features of signs and symptosm?

A 
Presence of risk factors
Bradykinesia
Resting tremor
Rigidity
Postural instability
169
Q

What are the other diagnostic features of parkinson’s disease?

A 
Masked facies
Hypophonia
Hypokinetic
Micrographia
Stooped posture
Shuffling gait
Conjugate gaze disorders
Fatigue
Constipaiton
Depression
Anxiety 
Dementia
170
Q

What are the uncommon features of parkinson’s disease?

A

Exposure to Neuroleptics or antiemetics

Featrues of atypical parkinsonism (Acute onset, rapid progression, cognitive impairment)

171
Q

What are the investigations for Parkinson’s disease?

A

Dopaminergic agent trial (improved symptoms)
MRI brain (normal)
Functional neuroimaging
Olfactory testing
Brain pathology
Genetic testing
Lewy bodies and positive reactivity to synuclein with immunohistochemical staining

172
Q

What is Radiculoapthy?

A

Spinal nerve root compression

173
Q

What are the most common types of radiculopathy?

A

Lumbar and cervical radiculopathy

174
Q

What are the causes of radiculopathy?

A 
Herniated disc
Spinal stenosis
Degenerative disc disease
Osteoarthritis
Facet joint degeneration/hypertrophy
LIgamentous hypertrophy
Spondylolisthesis (vertebra moves and rests on vertebrae below)
Rarer: Radiation, DM, Neoplastic disease, lyme meningitis
175
Q

What are the risk factors for radiculopathy?

A 
Age
Overweight
Poor posture
Improper lifting technique
Family history of degenerative bone conditions
176
Q

What are the signs and symptoms of radiculopathy?

A

Lumbar or sacral radiculopathy (primary sciatica)
Pain/electrical sensations in arms or fingers or legs at level of compression
Dull reflexes
Dynatomal sensory disturbance (numbness, tingling, reduced pain and temperature sensation)
LMN weakness and eventual muscle wasting
UMN signs below affected level (Spasticity, weakness, brisk reflexes and upgoing plantars)
Position and vibration sense may be lost

177
Q

What are the investigations for Radiculopathy?

A 
Full Neurological exam
MRI
X-ray and MRI
EMG to test nerve function
Nerve conduction studies
178
Q

What is Raised intracranial pressure?

A

The volume inside the cranium is fixed so any increase in the contents can lead to raised ICP/ Can be mass efect, oedema or obstruction to fluid outflow
Normal ICP in adults is <15mmHg

179
Q

What causes raised intracranial pressure?

A 
Primary or metastatic tumours
Head injury
Haemorrhage
Infection (Meningitis, encephalitis, brain abscesses)
Hydrocephalus
Cerebral oedema
Status epilepticus 
Aneurysms
180
Q

What are the symptoms of a raised ICP?

A 
Headache (worse on coughing and leaning forward, worse in morning)
Vomiting
Altered GCS
History of trauma
Poor vision
181
Q

What are the signs of a raised ICP?

A

Altered GCS
Falling pulse and rising BP (Cushing’s response)
Cheyne-Stokes respiration
Pupil changes
Reduced visual acuity
peripheral visual field loss
Papilloedema (unreliable sign but venous pulsaiton of disc may be absent)

182
Q

What is Cheyne-stokes respiration?

A

Progressively deeper and sometimes faster breathing followed by a gradual decrease that results in a temporary stop in breathing

183
Q

What are the investigations for Raised ICP?

A 
U&amp;Es
FBC
LFT
Glucose
Serum osmolality
Clotting
Blood culture
Consider toxicology screen
CXR
CT head
Consider LP if safe
184
Q

What is spinal cord compression?

A

Pressure injury to the spinal cord with Neurological symptoms dependent on site and extent of the injury

185
Q

What is Cauda equina syndrome?

A

Symptoms due to damage to the bundle of nerves below the end of the spinal cord (L2 down)

186
Q

What is conus medullaris syndrome?

A

Tapered, lower end of the spinal cord i the conus medullaris.
Conus medullaris syndrome is compression at L1/L2

187
Q

What causes spinal cord compression?

A 
Most causes: Trauma and tumours
Tumours are more frequently metastases
Spinal abscess
TB (Pott's disease)
Haematoma (warfarin)
Intrinsic cord tumour
Atlanto-axial sublulxation
Myeloma
Congenital lumbar disc disease
188
Q

What are the risk factors for spinal cord compression?

A 
Trauma
Malignancy
Osteoporosis
Metabolic bone disease
Vertebral disc disease
189
Q

What are the symptoms of spinal cord compression?

A 
History of trauma or malignancy
Pain 
Weakness
Sensory loss
Disturbance of bowel and bladder function
190
Q

What are the signs of spinal cord compression?

A 
Normal above lesions
Diaphragmatic breathing
Reduced anal tone
Hyporeflexia
Priapism
Spinal shock
Sensory loss (level of lesion)
Motor 
- Weakness or paralysis 
- Downward plantars (acute)
- UMN signs below lesions
- LMN signs at level of lesion
191
Q

What is Brown-Sequard syndrome?

A

Seen with hemisection of spinal cord

192
Q

What are the investigations for spinal cord compression?

A

Radiology
- Lateral radiographs of spine to look for loss of alignment, fractures etc
- MRI
Bloods
- FBC, U&E, Calcium, ESR, Immunoglobulin electrophoresis (Multiple Myeloma), syphilis serol, LFTs, PSA
- CXR for lung malignancy, TB
- Urine (Bence Jones proteins - multiple myeloma)

193
Q

What is a stroke?

A

Acute neurological deficit of two different types

194
Q

What are the types of stroke?

A

Ischaemic or Haemorrhagic

195
Q

What is an ischaemic stroke?

A

Acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology caused by vascular occlusion or stenosis.
Resulting in intraparenchumal and/or subarachnoid haemorrhage

196
Q

What is a Haemorrhagic stroke?

A

Acute neurological deficit caused by cerebrovascular aetiology. Due to a rupture of a cerebrospinal artery, resulting in intraparenchymal subarachnoid and intraventricular haemorrhage

197
Q

What causes an ischaemic stroke?

A

Transient of permanent critical reduction in cerebral blood flow due to arterial occlusion, Hypotension, vasculitis or cocaine

198
Q

How does thrombosis cause ischaemic strokes?

A

Lacunar infarcts (Small vessels)
Can occur in larger vessels (middle cerebral artery)
Can arise in prothrombotic states (e.g. dehydration, thrombophilia)

199
Q

How does an embolus cause ischaemic stroke?

A

Carotid dissection
Carotid atherosclerosis
AF

200
Q

What causes a haemorrhagic stroke?

A 
Hypertension
Charcot-Bouchard microaneurysm rupture
Amyloid angiopathy
Arteriovenous malformaitons
Anticoagulant therapy
Trauma
Tumours
Vasculitis
201
Q

What are the risk factors for ischaemic stroke?

A 
Older age
Family history
History of stroke
Hypertension
Smoking
Diabetes mellitus
Atrial fibrillaiton
Comorbid cardiac conditions
Carotid artery stenosis
Sickle cell disease
Dyslipidaemia
People with lower levels of education
Obesity
Elevated CRP
Aortic arch plaques
202
Q

What are the risk factors for haemorrhagic stroke?

A 
Hypertension
Advanced age
Male sex
Asian, black and/or hispanic
Family history of heamorrhagic stroke
Asian, black or hispanic 
Haemophilia
Smoking
Illicit sympathomimetic drugs
Leukaemia
Thrombocytopeina
AD mutaitons
Hereditary haemorrhagic telangiectasia
Leukaemia
Moyamoya disease
NSAID
203
Q

What are the symptoms of ischaemic stroke?

A 
Sudden onset
Vision loss or visual field deficit
Impaired co-ordination
Loss of function
Diplopia
Sensory loss
Vertigo/dizziness
Nausea and / or vomiting
Confusion
altered sensation
Headahce
Neck/facial pain
204
Q

What are the signs of ischaemic stroke in the anterior cerebral artery?

A

Hemiparesis
Confusion
Disturbance of intellect, executive function, judgement and social behaviour

205
Q

What are the signs of ischaemic stroke in the middle cerebral artery?

A 
Facial weakness
Hemiparesis
Hemisensory loss
Apraxia
Hemineglect
Aphasia if left sided 
Hemineglect
Quadrantopia
206
Q

What are the signs of ischaemic stroke in the posterior cerebral artery?

A

Homonymous hemianopia, visual agnosia

207
Q

What are the symptoms of haemorrhagic stroke?

A 
Neck stiffness
History of AF
History of liver disease
Altered sensation
weakness
Headache
Sensory loss
Aphasia
Dysarthria
Ataxia
Vertigo
Nausea/vomiting
Confusion
Gaze paresis
Altered consciousness
208
Q

What are the signs of haemorrhagic stroke?

A 
Meningism
Severe headache
Coma within hrs
Carotid bruit
AF
previous TIA
IHF
209
Q

What investigations are done for ischaemic stroke?

A 
FBC 
Serum glucose (normal)
Serum electrolytes (normal)
Serum U&amp;Es (Normal)
Cardiac enzymes (normal)
PTT/aPTT (Normal/coagulopahty)
Toxicology screen 
ESR
Carotid doppler US
CT head MRI brain ECG
CXR
CT cerebral angiogram
210
Q

What are the investigations for haemorrhagic stroke?

A 
Chemistry panel (normal)
CBC (exclude thrombocytopenia)
Clotting test
Platelet function test
LFT 
Non-infused CT
ECG
CT angiography and venography
MR angiography and venography
MRI brain with diffusion-weighted imaging adn gradient echo sequence
211
Q

What is the management for stroke?

A

<4.5 hrs since onset:

  • CT Head to exclude haemorrhage
  • IV alteplase
  • Aspirin 24 hrs later

> 4.5hrs since onset;

  • 300mg Aspirin (heparin if high emboli recurrence)
  • Swallow assessment
  • Thromboprophylaxis

Secondary:

  • clopidogrel / aspirin 75mg
  • warfarin if paroxysmal AF
  • control risk factors

Surgical:
Carotd endarterectomy

212
Q

What are the complications of stroke?

A 
Aspiration pneumonia
Cerebral oedema
Immobility
Infections
DVT
Cardiovascular events
Death
213
Q

What is a subarachnoid haemorrhage?

A

Arterial haemorrhage into the subarachnoid space

214
Q

What causes a subarachnoid haemorrhage?

A

Rupture of a saccular aneurysms at base of brain (berry aneurysm) - 85%
Perimesencephalic haemorrhage - 10%
Arteriovenous malformations, bleeding diathesis, vertebral artery dissection - 5%

215
Q

What are the risk factors for a subarachnoid haemorrhage?

A 
Hypertension
Smoking
Excessive alcohol intake
Bleeding disorders
Family history of SAH
Saccular aneurysms
216
Q

What are saccular aneursysms associated with?

A 
PKD
Coarctation of he aorta
Marfan's syndrome
Ehlers-Danlos syndrome
SLE
217
Q

What are the symptoms of SAH?

A 
Sudden-onset worst headache ever
Nausea/vomiting
Collapse
Seizures
Neck stiffness
Photophobia
Reduced level of consciousness
218
Q

What are the sign’s of SAH?

A

Meningism (Neck stiffness, kernig’s sign, pyrexia)
GCS - Check for deterioration
Signs of raised ICP
- Papilloedema, CN IV/III palsies, HTN, bradycardia, focal neurological signs

219
Q

What investigations are done for SAH?

A 
FBC (Leucocytosis)
INR (Raised)
PTT (Raised)
Troponin (High)
CT scan asap
if inconclusive - LP (increased pressure, incerased red cells, blood then xanthochromia)
ECG: 50% have an abnormal ECG
220
Q

What is a Subdural haemorrhage?

A

A collection of clotting blood that forms in the subdural space

221
Q

What are the 3 classifications of subdural haemorrhage?

A

Acute
Subacute (3-7 days after)
Chronic (2-3 weeks after)

222
Q

Who are the at risk groups of SDH?

A

Infants
Elderly
Alcoholics
People on anticoagulation treatment

223
Q

What causes SDH?

A

Trauma

Less commonly: Rupture of aneurysm or vascular malformations

224
Q

What are the risk factors for SDH?

A

Recent trauma
Coagulopathy and anticoagulant use
Advanced age (>65)

225
Q

What are the symptoms of acute SDH?

A

History of trauma

Reduced consciousness level

226
Q

What are the symptoms of subacute SDH?

A

Worsening headache 7-14 days after injury

Altered mental state

227
Q

What are the symptoms of chronic SDH?

A 
Headache
Confusion
Cognitive impairment
Gait deterioration
Focal weakness
Seizures
Sleepiness
228
Q

What are the signs of acute SDH?

A 
Reduced GCS
Ipsilateral fixed dilated pupil 
Pressure on brainstem (reduced consciousness + bradycardia)
Evidence of trauma
Papilloedema
229
Q

What are the signs of chronic SDH?

A

Neurological examination may be normal
Focal neurological signs (3rd nerve palsy)
Evidence of trauma
Papilloedema

230
Q

What investigations are done for SDH?

A 
FBC
U&amp;Es
LFTs
Thrombocytopenia
Coagulation screen
Cross-match/Group and save
CT head
C-spine imaging
231
Q

What is the management of acute SDH?

A 
ALS protocol
Watch out for C-spine injury
Raised ICP consider osmotic diuresis
Conservative if small
Surgical (for irrigation/evacuation)
- Burr twist drill and burr hole craniotomy
- Craniotomy
232
Q

What is the management for chronic SDH?

A

Burr hole or craniotomy and drainage
Assess any causes of trauma
Children - treat with percutaneous aspiration via open fotanelle

233
Q

What are complications of SDH?

A 
Neurological deficits
Come
Stroke
Surgical-site infection
Epilepsu
Recurrence of SDH postoperatively
234
Q

What is a tension headache?

A

Generalised headache throughout the head with a predilection for involving the frontal and occipital regions.
Pain expressed as being a ‘tight-band’ around the head
TTH can be episodic or chronic

235
Q

What causes tension headache?

A

Muscle contraction considered cause of pain
Stress most common trigger
Disturbed sleep patterns can trigger episodic headache
Insomnia and other sleep disorders are associated with chronic headache

236
Q

What are the risk factors for headaches?

A 
Mental tension
Stress
Missing meals
Fatigue
Somatisation
Female sex
20-39 years old
Lower socioeconomic status 
Analgesic overuse
237
Q

What are the signs and symptoms of tension headache?

A

Pressure or tightness
Related to neck pain
Non-pulsatile head pain
Often photophobia and exacerbation by movement are common
Mild nausea may occur
Head pain, frontal or occipital head pain

238
Q

What are the investigations for tension headache?

A

Not needed but can do CT sinus, MRI brain and LP which would all be normal

239
Q

What is the management for tension headaches?

A

Reassure positive diagnosis
Attention to stress, anxiety or depression
Physiotherapy for mobilisation
Advice on opioids/medications

Simple analgesia
- Ibuprofen fine, possibly paracetamol or naproxen, aspirin
TCA
- Amitriptyline

240
Q

What is a TIA?

A

Episode where someone has signs or symptoms of a stroke but they only last a short amount of time.
Usually last a few minutes - few hours

241
Q

What are the risk factors for TIA?

A 
Diabetes
Age >40 
Severely clogged or narrowed arteries
Obesity
Heart disease
Illegal drug use or heavy alcohol use
Recent childbirth
Sedentary lifestyle/lack of exercse
Current or past history of blood clots
High blood cholesterol
242
Q

What are the signs and symptoms of TIA?

A

Single or many attacks
Similar in the arterial area to a stroke there
Amaurosis fugax if goes to retinal artery
May have limb-shaking
Syncope, dizziness not typical in TIAs

243
Q

What are the investigations for TIA?

A 
Blood glucose (<3.3)
U&amp;Es (Low Na+, K+ or High Ca2+)
FBC (possibly raised, polycythaemia, thrombocytopenia)
Brain MRI [First line]
CXR
244
Q

How do you manage TIA?

A

ABCD2 assessment
- If = 3: Aspirin or clopidogrel adn a statin
- If >/= 4: Aspirin or clopidogrel, measure for secondary CVS prevention
Those with AF should be anticoagulated
Cardiac emboli / Af need warfarin

Carotid endarterectomy if >/= 70% stenosis on internal carotid

245
Q

How does a TIA affect their ability to drive?

A 
Group 1 (Car/motorcycle):
- Not drive for a month, no need to tell DVLA for 1 TIA, multiple needs 3 months off
Group 2 (lorry or bus):
- Licence refused/revoked for a year
246
Q

What are the complications for TIAs?

A

Stroke

Myocardial infarction

247
Q

What is trigeminal Neuralgia?

A

Neuralgia involving one or more of the brances of the trigeminal nerves, often causing severe pain

248
Q

What triggers trigeminal Neuralgia?

A 
Vibration
Skin contact
Eating
Talking
Dental protheses
Brushing teeth
Exposure to wind
249
Q

What causes trigeminal neuralgia?

A

Thought to be due to compression of the trigeminal nerve by a loop of artery or vein
Secondary causes (5-10%)
Can be MS or Brainstem lesions but thats rare
Compression of the trigeminal root by anomalous or aneurysmal intracranial vessels or a tumour

250
Q

What are risk factors for trigeminal neuralgia?

A

Increased age

MS

251
Q

What are the signs and symptoms of trigeminal neuralgia?

A

Sudden u/l stabbing pain in distribution of one or more of the branches of the trigeminal nerve
Recurrent
Lasts from a few seconds to a couple of mins
Periods of reission may vary
Pain is decribed a being shock-like (Face screws with pain)

252
Q

What are the investigations for Trigeminal neuralgia?

A

Diagnosis is clinical

MRI needed to exclude secondary diagnosis

253
Q

What is Wernicke’s encephalopathy?

A

Presence of Neurological symptoms caused by biochemical lesions of the CNS following exhaustion of Vitamin B reserves

254
Q

What causes wernicke’s encephalopathy?

A 
Main cause is alcohol consumption which results in thiamine deficiency by causing:
- Inadequate nutritional thiamine intake
- Decreased thiamine absorption
- Impaired thiamine utilisation by cells
Other causes:
- Eating disorders
- Malnutrition
- Prolonged vomiting
- GI malignancy
- Chronic subdural haematoma
- AIDS
- Hyperemesis gavidarum
- Thyrotoxicosis
255
Q

What is Hyperemesis gravidarum?

A

Severe nausea, vomiting, weight loss in pregnancy

256
Q

What are the risk factors for Wernicke’s encephalopathy?

A 
Alcohol dependence 
AIDS
Cancer treatment
Malnutrition/eating disorder
History of GI surgery
257
Q

What are the symptoms of wernicke’s encephalopathy?

A

Vision changes
Loss of muscle coordination
memory loss/change
Hallucinations

258
Q

What are the signs of Wernicke’s encephalopathy?

A 
Triad
- Confusion
- Ophthalmoplegia
- Ataxia
Patients are mentally alert with vocabulary, comprehension, motor skills, social habits and naming ability maintained
You will see:
- Decreased reflexes/temperature
- Rapid pulse
Korsakoff's psychosis:
- Amnesia
- Confabulation (made-up stories fill any gaps in memory)
259
Q

What investigations are done for wernicke’s encephalopathy?

A

Clinical diagnosis

  • Parenternal thiamine (improvement)
  • Renal function
  • FBC
  • Electrolytes
  • Glucose
  • Ammonia
  • LFTs
  • Magnesium (Low)

conditions (18 decks)

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