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Neurology Flashcards

1
Q

What is papilloedema?

A
  • swollen optic nerve causing visual disturbances, headaches and nausea - is a ophthalmology emergency
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2
Q

Define Bell’s palsy.

A

Idiopathic lower motor neurone facial nerve palsy.

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3
Q

What are the risk factors for Bell’s palsy?

A

o IDIOPATHIC

  • however, 60% are preceded by an upper respiratory tract infection -> suggests that it has a viral or post-viral aetiology
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4
Q

What are the presenting symptoms of Bell’s palsy?

A

Unilateral facial weakness and droop

50% experience facial, neck or ear pain or numbness

Hyperacuisis (due to stapedius paralysis)

Loss of taste (uncommon)

Tearing or drying of exposed eye

  • some cases experience prodrome pre-auricular pain
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5
Q

What are the signs of Bell’s palsy on examination?

A

o Lower motor neurone weakness of facial muscles - affects ipsilateral muscles of facial expression

o Bell’s Phenomenon - eyeball rolls up but the eye remains open when trying to close their eyes

o Despite unilateral facial numbness, clinical testing of sensation is normal

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6
Q

How do upper and lower motor neurone palsy’s of CN 6 differ?

A

o Lower (Bell’s) does NOT spare the muscles of the upper part of the face unlike upper motor neurone facial nerve palsy

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7
Q

What are the appropriate investigations for Bell’s palsy?

A

o Usually unnecessary (except for excluding other causes)

  • EMG - may show local axonal conduction block
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8
Q

What is the treatment for Bell’s palsy?

A

o 85-90% make a full recover in 2-12 weeks without treatment

  • Protection of cornea with protective glasses/patches or artificial tears
  • High-dose corticosteroids is useful within 72 hrs (if Ramsey-Hunt Syndrome is excluded)
  • Surgery - lateral tarsorrhaphy (suturing the lateral parts of the eyelids together)
  • all eye orientated
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9
Q

What is Ramsey-Hunt syndrome?

A

An acute peripheral facial neuropathy associated with erythematous vesicular rash of the skin of the ear canal, auricle (also termed herpes zoster oticus), and/or mucous membrane of the oropharynx.

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10
Q

What are the possible complications of Bell’s palsy?

A

o Corneal ulcers

o Eye infection

o Aberrant reinnervation -> blinking may cause contraction of the angle of the mouth due to aberrant sympathetic innervation of orbicularis oculi and oris

o Crocodile Tears Syndrome - parasympathetic fibres may aberrantly reinnervate the lacrimal glands causing tearing whilst salivating

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11
Q

Define cluster headache.

A

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 several weeks.

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12
Q

What are the risk factors for cluster headaches?

A
  • genetics
  • being male
  • 20-40 years of age
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13
Q

Define episodic cluster headaches.

A

Cluster headaches occurring in periods lasting 7 days - 1 year, separated by pain-free periods lasting a month or longer.

Cluster periods usually last between 2 weeks - 3 months.

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14
Q

Define chronic cluster headaches.

A

Cluster headaches occurring for 1 year without remissions or with short-lived remissions of less than a month.

Chronic cluster headaches can arise de novo or arise from episodic cluster headaches.

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15
Q

Describe the pattern of occurrence of cluster headaches.

A

o Headaches occur in bouts lasting 6-12 weeks - tend to occur at the same time each year

o Headaches typically occurs at night, 1-2 hours after falling asleep

o The interval between bouts tends to be the same

o 10% with episodic cluster headaches go on to develop chronic cluster headaches

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16
Q

What are the presenting symptoms of cluster headaches?

A

o Intense, sharp, penetrating pain comes on rapidly over around 10 mins

o Pain is unilateral and centred around the eye, temple or forehead

o Associated autonomic features: ipsilateral lacrimation, rhinorrhoea, nasal congestion, eye lid swelling, facial swelling, flushing, conjunctival injection, partial Horner’s syndrome

o Patients find it difficult to stay still and will pace around, occasionally banging their heads on things

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17
Q

What are the triggers of cluster headaches?

A

ALCOHOL - major precipitant

Exercise and solvents

Sleep disruption

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18
Q

What are the appropriate investigations for cluster headaches?

A

CLINICAL diagnosis based on history

Neurological examination may be useful

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19
Q

Define dementia.

A

A chronic and progressive deterioration of cognitive function due to organic brain disease. It is irreversible and consciousness is not impaired.

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20
Q

What are the 4 types of dementia?

A

Alzheimer’s disease (50%) - degeneration of the cerebral cortex, with cortical atrophy and reduction in acetylcholine production

Vascular Dementia (25%) - brain damage due to several incidents of cerebrovascular disease (e.g. strokes/TIAs)

Lewy Body Dementia (15%) - deposition of abnormal proteins (Lewy bodies) within the brain stem and neocortex

Frontotemporal Dementia - specific degeneration of the frontal and temporal lobes

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21
Q

Describe Alzheimer’s.

A
  • degeneration of the cerebral cortex, with cortical atrophy and reduction in acetylcholine production
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22
Q

Describe vascular dementia.

A
  • brain damage due to several incidents of cerebrovascular disease (e.g. strokes/TIAs)
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23
Q

Describe Lewy Body dementia.

A
  • deposition of abnormal proteins (Lewy bodies) within the brain stem and neocortex
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24
Q

What are the presenting symptoms of dementia?

A
  • a progressive loss of memory and cognitive function
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25
Q

How does Alzheimer’s present?

A
  • insidious onset of memory and cognitive function decline
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26
Q

How does vascular dementia present?

A
  • step-wise onset of memory and cognitive function decline
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27
Q

How does Lewy Body dementia present?

A
  • fluctuating levels of consciousness, hallucinations, falls and Parkinsonian symptoms along with memory and cognitive decline
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28
Q

How does frontotemporal dementia present?

A
  • behavioural changes and intellectual changes along with memory and cognitive decline
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29
Q

What are the appropriate investigations for dementia?

A

Diagnosis is based on the HISTORY

  • ensure no treatable cause is missed (e.g. hypothyroidism, vitamin B12/folate deficiency, space-occupying lesion, normal pressure hydrocephalus)
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30
Q

Define Guillain-Barre syndrome.

A

Acute inflammatory demyelinating polyneuropathy.

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31
Q

What is the risk factors for Guillain-Barre syndrome?

A

o An inflammatory process where antibodies after a recent infection react with self-antigen on myelin or neurons

o 40% of cases are idiopathic

Other causes: malignancy (e.g. lymphoma) or post-vaccination

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32
Q

What are the presenting symptoms of Guillain-Barre syndrome?

A

o Progressive symptoms of ascending symmetrical limb weakness and ascending paraesthesia

o Cranial nerve involvement (dysphagia, dysarthria, facial weakness)

o Respiratory muscles may be affected in SEVERE cases

o Miller-Fisher Variant (RARE) = ophthalmoplegia, ataxia, arreflexia

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33
Q

What are the signs of Guillain-Barre syndrome on examination?

A

o General motor examination = hypotonia, flaccid paralysis, arreflexia (ascending upwards from feet to head)

o General sensory examination = impairment of sensation in multiple modalities (ascending from feet to head)

o Cranial nerve palsies = facial nerve weakness, abnormality of external ocular movements, if pupil constriction is affected consider botulism

o Type II respiratory failure = due to paralysis of respiratory muscles

o Autonomic function = assess postural blood pressure change and arrhythmias

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34
Q

What are the appropriate investigations for Guillain-Barre syndrome?

A

o Lumbar puncture = high protein with normal cell count and glucose

o Nerve conduction study = reduced conduction velocity

o Bloods = anti-ganglioside antibodies in Miller-Fisher variant + 25% of Guillain-Barre cases

o Spirometry = reduced fixed vital capacity - suggests ventilatory weakness

o ECG = arrhythmias may develop

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35
Q

Define Horner’s syndrome.

A

A condition that results from the disruption of the sympathetic nerves supplying the face resulting in a triad of:

Ptosis

Miosis

Anhydrosis

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36
Q

What are the causes of Horner’s syndrome?

A

Caused by disruption of the sympathetic nerves

  • Strokes
  • Multiple sclerosis
  • Apical lung tumours
  • Lymphadenopathy
  • Basal skull tumours
  • Carotid artery dissection
  • Neck trauma
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37
Q

What are the presenting symptoms of Horner’s syndrome?

A

Inability to open the eye fully on the affected side

Loss of sweating on affected side

Facial flushing

Orbital pain/headache

Other symptoms based on cause

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38
Q

What are the signs of Horner’s syndrome on examination?

A

Ptosis

Miosis

Anhydrosis

Enophthalmos

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39
Q

What are the appropriate investigations for Horner’s syndrome?

A

Investigations are directed towards figuring out the underlying cause

CXR - apical lung tumour

CT/MRI - cerebrovascular accidents

CT angiography - dissection

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40
Q

What is the treatment for Horner’s syndrome?

A

Horner’s syndrome is a sign not a disease in itself

So, the management depends on the cause (e.g. management for carotid dissection is very different to management of apical lung tumours)

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41
Q

Define Huntington’s disease.

A

Autosomal dominant trinucleotide repeat disease characterised by progressive chorea and dementia, typically commencing in middle age.

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42
Q

What are the presenting symptoms of Huntington’s disease?

A

o FAMILY HISTORY

o Insidious onset in middle-age

o Progressive

o Fidgeting

o Clumsiness

o Involuntary, jerky, dyskinetic movements often accompanied by grunting and dysarthria

o Early cognitive changes = lability, dysphoria (a state of unease or generalised dissatisfaction with life), mental inflexibility, anxiety, develops into dementia

o Later stages = rigid, akinetic, bed-bound

o Enquire about drug history (especially cocaine and anti-psychotics)

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43
Q

What are the signs of Hungtinton’s disease on examination?

A

Chorea

Dysarthria

Slow voluntary saccades

Supranuclear gaze restriction

Parkinsonism

Dystonia

MMSE shows cognitive and emotional deficits

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44
Q

What are the appropropriate investigations for Huntington’s disease?

A

o Genetic analysis = diagnostic if there are > 39 CAG repeats in the HD gene and reduced penetrance leads to an intermediate number of CAG repeats

o Imaging = brain MRI or CT may show symmetrical atrophy of the striatum and butterfly dilation of the lateral ventricles

o Bloods = exclude other pathology

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45
Q

Define hydrocephalus.

A

Enlargement of the cerebral ventricular system.

  • can be subdivided into obstructive and non-obstructive (aka communicating and non-communicating)
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46
Q

Define hydrocephalus ex vacuo.

A

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

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47
Q

Describe the distribution of people who suffer from hydrocephalus.

A

YOUNG - congenital malformations and brain tumours

ELDERLY - strokes and tumours

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48
Q

What are the presenting symptoms of obstructive hydrocephalus?

A

Acute drop in conscious level

Diplopia/double vision

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49
Q

What are the presenting symptoms of normal pressure hydrocephalus?

A

Dementia

Gait disturbance

Urinary incontinence

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50
Q

What are the signs of obstructive hydrocephalus on examination?

A

o Low GCS

o Papilloedema

o 6th nerve palsy (longest CN so most susceptible to raised ICP)

o NEONATES - increased head circumference and sunset sign (downward conjugate deviation of the eyes)

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51
Q

What are the signs of normal pressure hydrocephalus on examination?

A

Cognitive impairment

Gait apraxia (shuffling)

Hyperreflexia

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52
Q

What are the appropriate investigations for hydrocephalus?

A

o CT Head = FIRST-LINE for detecting hydrocephalus -> may also pick up the cause (e.g. tumour)

o CSF/Ventricular drain/Lumbar puncture - may indicate pathology (e.g. tuberculosis),check MC&S, protein and glucose

  • lumbar puncture -> contraindicated if raised ICP and therapeutic in normal pressure hydrocephalus
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53
Q

Define migraine.

A

Severe episodic headache that may have a prodrome of focal neurological symptoms (aura) and is associated with systemic disturbance.

54
Q

What are the risk factors for migraines?

A
  • being female
  • age = adolescence and early adulthood
55
Q

What are the presenting symptoms of migraines?

A

o Headache = pulsatile, duration of 4-72 hrs, episodic

o Associated symptoms = nausea, vomiting, photophobia/phonophobia, aura (flashing lights, spots, blurring, zigzag lines, blind spots (scotomas), tingling/numbness in the limbs)

56
Q

Name some triggers of migraines.

A

Stress

Exercise

Lack of sleep

Oral contraceptive pill

Foods (e.g. caffeine, alcohol, cheese, chocolate)

57
Q

What are the signs of migraine on examination?

A

NO specific physical findings

Exclude secondary causes with MMSE, neurological examination, fundoscopy etc.

58
Q

What are the appropriate investigations for migraines?

A

Diagnosis is usually based on HISTORY

Investigations may be useful for excluding other diagnoses - Bloods, CT/MRI, lumbar puncture

59
Q

What is the treatment plan for migraines?

A

o Acute = NSAIDs, paracetamol, codeine, anti-emetics, t

o Prophylaxis = b-blockers, amitriptyline, topiramate, sodium valproate, oral contraceptive pill (for menstrual migraines)

o Advice = avoid triggers, rest in a quiet dark room during episodes

NOTE: analgesia overuse can cause headaches

60
Q

What are the possible complications of migraines?

A

Disruption of daily activities

Can lead to analgesia-overuse headaches in people who use analgesia regularly

61
Q

Define motor neurone disease.

A

A progressive neurodegenerative disorder of cortical, brainstem and spinal motor neurons (lower and upper motor neurons).

62
Q

What are the subtypes of motor neurone disease?

A

Amyotrophic Lateral Sclerosis (ALS)

Progressive Muscular Atrophy Variant

Progressive Bulbar Palsy Variant

Primary Lateral Sclerosis Variant

63
Q

What is ALS?

A

o Amyotrophic Lateral Sclerosis (ALS)

  • combined degeneration of upper AND lower motor neurones resulting a mix of LMN and UMN signs
64
Q

What is progressive muscular atrophy variant?

A

Only LMN signs

Better prognosis

65
Q

What is progressive bulbar palsy variant?

A

Dysarthria

Dysphagia

Wasted fasciculating tongue

Brisk jaw jerk reflex

66
Q

What is primary lateral sclerosis variant?

A

UMN pattern of weakness

Brisk reflexes

Extensor plantar responses

NO LMN signs

67
Q

What are the possible complications of motor neurone disease?

A

Frontotemporal lobar dementia

68
Q

What are the presenting symptoms of motor neurone disease?

A

Weakness of limbs

Speech disturbance

Swallowing disturbance

Behavioural changes

69
Q

What are the signs of motor neurone disease on examination?

A

o Combination of UMN and LMN signs

  • LMN Features = muscle wasting, fasciculations , flaccid weakness, hyporeflexia
  • UMN Features = spastic weakness, extensor plantar response, hyperreflexia

o Sensory examination = should be normal

o possibly a family history of MND (5-10% autosomal dominant)

70
Q

What are the appropriate investigations for MND?

A

o Bloods = mild elevation in CK, ESR, anti-GM1 ganglioside antibodies

o Electromyography (EMG) = nerve conduction studies = often normal

o MRI to exclude cord compression and brainstem lesions

o Spirometry to assess respiratory muscle weakness

71
Q

Define MS.

A

Inflammatory demyelinating disease of the CNS.

72
Q

What are the types of MS?

A

o Relapsing-Remitting MS = COMMONEST form = clinical attacks of demyelination with complete recovery in between attacks

o Primary Progressive MS = steady accumulation of disability with NO relapsing-remitting pattern

o Marburg Variant = severe fulminant variant of MS leading to advanced disability or death within weeks

o Clinically Isolated Syndrome = single clinical attack of demyelination which itself does NOT count as MS -> 10-50% progress to develop MS

73
Q

What are the risk factors for MS?

A
  • EBV exposure
  • low prenatal vitamin D levels
74
Q

What are the presenting symptoms of MS?

A

o Varies depending on the site of inflammation

o Optic Neuritis (commonest) = unilateral deterioration of visual acuity and colour perception, pain on eye movement

o Sensory = pins and needles, numbness, burning

o Motor = limb weakness, spasms, stiffness, heaviness

o Autonomic = urinary urgency, hesitancy, incontinence, impotence

o Psychological = depression, psychosis

o Uhthoff’s Sign = worsening of neurological symptoms as the body gets overheated from hot weather, exercise, saunas, hot tubs etc.

o Lhermitte’s Sign = an electrical sensation that runs down the back and into the limbs when the neck is flexed

75
Q

What is Uhthoff’s sign?

A
  • worsening of neurological symptoms as the body gets overheated from hot weather, exercise, saunas, hot tubs etc.
76
Q

What is Lhermitte’s sign?

A
  • an electrical sensation that runs down the back and into the limbs when the neck is flexed
77
Q

What are the signs of MS on examination?

A

o Optic Neuritis = impaired visual acuity, loss of coloured vision

o Visual Field Testing = central scotoma, field defects

o Relative Afferent Pupillary Defect (RAPD)

o Internuclear Ophthalmoplegia = lateral horizontal gaze causes failure of adduction of the contralateral eye -> indicates lesion of the contralateral medial longitudinal fasciculus

o Sensory = paraesthesia

o Motor = UMN signs

o Cerebellar = limb ataxia (intention tremor, past-pointing, dysmetria), dysdiadochokinesia, ataxic wide-based gait, scanning speech

78
Q

What are the appropriate investigations for MS?

A

o Diagnosis is based on the finding of two or more CNS lesions with corresponding symptoms, separated in time and space = McDONALD CRITERIA

o Lumbar Puncture to exclude infection/inflammatory causes and CSF electrophoresis shows unmatched oligoclonal bands

o MRI Brain, Cervical and Thoracic Spine (with gadolinium) so plaques can be identified

o Evoked potentials = visual, auditory and somatosensory evoked potentials may show delayed conduction velocity

79
Q

Define myasthenia gravis.

A

An autoimmune disease affecting the neuromuscular junction producing weakness in skeletal muscles.

80
Q

What is Lambert-Eaton syndrome?

A
  • paraneoplastic subtype of myasthenia gravis caused by autoantibodies against pre-synaptic calcium channels, leading to impairment of acetylcholine release
81
Q

What are the presenting symptoms of myasthenia gravis?

A

o Muscle weakness that worsens with repetitive use or towards the end of the day (muscle weakness improves after repeated use)

o Ocular symptoms - drooping eyelids, diplopia

o Bulbar symptoms - facial weakness (myasthenic snarl), disturbed hypernasal speech, difficulty smiling, chewing or swallowing

82
Q

What are the signs of mysathenia gravis on examination?

A

o Eye Signs = ptosis, complex ophthalmoplegia, ocular fatigue (ask the patient to sustain and upward gaze for 1 min and watch the progressive ptosis that develops), ice on eyes test (placing ice packs on closed eyelids for 2 mins can improve neuromuscular transmission and reduce ptosis)

o Bulbar Signs = reading aloud may cause dysarthria or nasal speech

o Limbs = test the power of a muscle before and after repeated use of the muscle

83
Q

What are the appropriate investigations for myasthenia gravis?

A

o Bloods = CK to exclude myopathies, serum acetylcholine receptor antibody (positive in 80%), TFTs as it is associated with hyperthyroidism, anti-voltage gated calcium channel antibody (in Lambert-Eaton syndrome)

o Tensilon Test = short-acting anti-cholinesterase increases acetylcholine levels and causes a rapid and transient improvement in clinical features however, there is a risk of bradycardia

o Nerve Conduction Study = repetitive stimulation shows decrements of muscle action potential

o EMG

o CT Thorax/CXR - visualise thymoma in the mediastinum or lung malignancies

84
Q

Define neurofibromatosis.

A

An autosomal dominant genetic disorder affecting cells of neural crest origin, resulting in the development of multiple neurocutaneous tumours.

85
Q

What are the types of neurofibromatosis?

A

o Type 1 Neurofibromatosis = peripheral and spinal neurofibromas, multiple café au lait spots, freckling (axillary/inguinal), optic nerve glioma, Lisch nodules (on iris), skeletal deformities, phaeochromocytomas, renal artery stenosis

o Type 2 Neurofibromatosis = Schwannomas (often bilateral vestibular schwannomas), meningiomas, gliomas, cataracts

86
Q

What are the presenting symptoms of type 1 neurofibromatosis?

A

o Positive family history - 50% are caused by new mutations

o Type 1 = skin lesions, learning difficulties (40%), headaches, disturbed vision (due to optic gliomas), precocious puberty (due to lesions of the pituitary gland from an optic glioma involving the chiasm)

87
Q

What are the presenting symptoms of type 2 neurofibromatosis?

A

o Positive family history - 50% are caused by new mutations

o Type 2 = hearing loss, tinnitus, balance problems, headache, facial pain and numbness

88
Q

What are the signs of type 1 neurofibromatosis on examination?

A

5+ café au lait macules of > 5 mm (prepubertal)

5+ café au lait macules of > 15 mm (post-pubertal)

Neurofibromas (may appear as cutaneous nodules or complex plexiform neuromas)

Freckling in armpit or groin

Lisch nodules (hamartomas on the iris)

Spinal scoliosis

89
Q

What are the signs of type 2 neurofibromatosis on examination?

A

Few or no skin lesions

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

90
Q

What are the appropriate investigations for neurofibromatosis?

A

Ophthalmological assessment

Audiometry

MRI brain and spinal cord - for vestibular schwannomas, meningiomas and nerve root neurofibromas

Skull X-ray (sphenoid dysplasia in NF1)

Genetic testing

91
Q

Define Parkinson’s disease.

A

Neurodegenerative disease of the dopaminergic neurones of the substantia nigra, characterised by Bradykinesia, Rigidity, Resting tremor and Postural instability.

92
Q

What are the types of Parkinson’s?

A

o Sporadic/Idiopathic Parkinson’s

o Secondary Parkinsons’s

93
Q

What are the risk factors for secondary Parkinson’s?

A

Neuroleptic therapy (e.g. for schizophrenia)

Vascular insults (e.g. in the basal ganglia)

MPTP toxin from illicit drug contamination

Post-encephalitis

Repeated head injury

94
Q

What are the presenting symptoms of Parkinson’s?

A

INSIDIOUS onset

Resting tremor (mainly in hands)

Stiffness and slowness of movements

Difficulty initiating movements

Frequent falls

Smaller hand writing (micrographia)

Insomnia

Mental slowness (bradyphenia)

95
Q

What are the signs of Parkinson’s on examination?

A

o Tremor - usually asymmetrical, decreased on action, pill rolling rest tremor, 4-6 Hz

o Rigidity - lead pipe rigidity of muscle tone, superimposed tremor can cause cogwheel rigidity, can be enhanced by distraction

o Gait - stooped, shuffling, small-stepped gait, reduced arm swing, difficulty initiating walking

o Postural instability - falls easily with little pressure from the back or the front

o Psychiatric - depression, cognitive problems and dementia (in later stages)

o Frontalis overactivation (leads to furrowing of the brow)

o Hypomimic face

o Soft monotonous voice

o Impaired olfaction

o Tendency to drool

o Mild impairment of up-gaze

96
Q

What are the appropriate investigations for Parkinson’s?

A

o CLINICAL diagnosis

o Levodopa Trial - timed walking and clinical assessment after administration

o Bloods - serum caeruloplasmin - rule out Wilson’s disease as a cause of Parkinson’s disease

o CT or MRI Brain - to exclude other causes of gait decline (e.g. hydrocephalus)

o Dopamine Transporter Scintigraphy - reduction in striatum and putamen

97
Q

Define spinal cord compression.

A

Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury.

98
Q

What are the causes of spinal cord compression?

A

o Trauma - leads to compression by - direct cord contusion, compression by bone fragments, haematoma, acute disk prolapse

o Tumours are more frequently METASTASES

o Other causes: spinal abscess, TB (Pott’s disease)

99
Q

What are the presenting symptoms of cord compression?

A

o History of trauma or malignancy

o Pain

o Weakness

o Sensory loss

o Disturbance of bowel and bladder function

o A large central lumbar disc prolapse may cause - bilateral sciatica, saddle anaesthesia (loss of sensation in the area of the buttocks covered by a bike seat), urinary retention

100
Q

What are the signs of cord compression on examination?

A

o Diaphragmatic breathing

o Reduced anal tone

o Hyporeflexia

o Priapism (persistent and painful erection)

o Spinal shock = low bp without tachycardia

o Sensory Loss - at level of the lesion

o Motor = weakness or paralysis, downward plantars (in acute phase), UMN signs below the level of the lesion, LMN signs at the level of the lesion

o Brown-Sequard Syndrome - seen with hemisection of the spinal cord

101
Q

What are the appropriate investigations for cord compression?

A

o Radiology = lateral radiographs of spine to look for loss of alignment, fractures etc.

o MRI or CT

o Bloods = FBC, U&Es, calcium, ESR, immunoglobulin electrophoresis (multiple myeloma)

o Urine = look for Bence Jones proteins (multiple myeloma)

102
Q

Define tension headache.

A

The most common type of headache, which is considered a ‘normal, everyday headache’.

103
Q

What are the categories of tension headaches?

A

o Episodic - occurs on < 15 days per month

o Chronic - occurs on > 15 days per month

104
Q

What are the causes/triggers of tensions headaches?

A

Stress/anxiety

Squinting

Poor posture

Fatigue

Dehydration

Missing meals

Bright sunlight

Noise

105
Q

What are the presenting symptoms of tension headaches?

A

o Mild-moderate in severity

o Pain is bilateral with pressure/tightness around the head like a tight band, often a relationship with the neck

o Can be disabling for a few hours but does not have specific associated symptoms (unlike migraines)

o Gradual onset with variable duration

o Usually responsive to over-the-counter medication

106
Q

What are the signs of tension headaches on examination?

A

o normal examination

107
Q

What is the treatment of tension headaches?

A

o Reassurance

o Address triggers (e.g. stress, anxiety)

o Advice on avoiding medications that can cause medication-induced headaches (e.g. opioids)

o Simple analgesia (e.g. ibuprofen, paracetamol, aspirin)

o Tricyclic antidepressants may be considered in frequently recurrent episodic tension headaches or chronic tension headaches

108
Q

Define TIA.

A

Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours.

109
Q

What are the risk factors for TIAs?

A

Hypertension

Smoking

Diabetes mellitus

Heart disease (valvular, ischaemic, atrial fibrillation)

Peripheral arterial disease

Polycythaemia rubra vera

COCP

Hyperlipidaemia

Alcohol

Clotting disorders

110
Q

What are the presenting symptoms of TIAs?

A

o History = TIAs usually last 10-15 mins (but can be anything from a few minutes to 24 hours)

o Clinical features depend on the part of the brain affected

  • Carotid Territory = unilateral, most often affect the motor area (weakness an arm, leg or one side of the face), dysarthria, Broca’s dysphasia (if Broca’s area is involved), amaurosis fugax (painless fleeting loss of vision caused by retinal ischaemia)

o Vertebrobasilar Territory = homonymous hemianopia, may be bilateral visual impairment, may be hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia or ataxia, ask about weakness, facial drooping, gait disturbance, confusion, memory loss, dysarthria or abnormal behaviour, check for simultaneous cardiac symptoms (e.g. palpitations)

111
Q

What are the signs of TIAs on examination?

A

Neurological examination may be normal because the TIA may have resolved by the time you do it

Check pulse for irregular rhythm (AF)

Auscultate the carotids to check for bruits (carotid atherosclerosis)

112
Q

What are the appropriate investigations for TIAs?

A

o Primary care investigations = urinalysis, FBC, U&Es, lipids, LFTs, TSH, ECG (may show AF or previous MI)

o Secondary care = unenhanced CT - if there is a possibility of a haemorrhage

o Investigate for source of emboli = ECG (24 hr tape or cardiac monitoring may be considered if paroxysmal atrial fibrillation is suspected), doppler ultrasound of carotid and vertebral arteries

113
Q

What are the treatments for TIAs?

A

o Patients with acute neurological symptoms that resolve completely within 24 hrs should be given 300 mg aspirin immediately and assessed urgently within 24 hrs

o Patients with confirmed TIA should receive = clopidogrel - 300 mg loading dose and 75 mg thereafter, high-Intensity statin therapy - e.g. atorvastatin 20-80 mg

o Secondary prevention = antiplatelets, antihypertensives, lipid-modifying treatments, management of AF

o Assessment of future stroke risk in TIA patients: ABCD2 score

114
Q

What is the ABCD2 score?

A
  • a scoring system for working out the likelihood of a stroke after a TIA
115
Q

Define trigeminal neuralgia.

A

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

116
Q

What are the causes of trigeminal neuralgia?

A

o Thought to be due to compression of the trigeminal nerve by a loop of artery or vein

o 5-10% of cases are thought to be due to tumours, MS or skull base abnormalities

117
Q

What are the presenting symptoms of trigeminal neuralgia?

A

o Sudden, unilateral, brief, stabbing pain in the distribution or one or more branches of the trigeminal nerve

o Recurrent, pain lasts from a few seconds to a couple of mins

o Periods of remission can vary

o Some experience preceding symptoms (e.g. numbness, tingling)

o Pain is described as being ‘shock-like’

118
Q

What are the triggers for trigeminal neuralgia?

A

Vibration

Skin contact

Brushing teeth

Oral intake

Exposure to wind

119
Q

What are the appropriate investigations for trigeminal neuralgia?

A

o Diagnosis is clinical

o If there is doubt over the underlying cause, specialists may request an MRI brain scan

120
Q

Define Wernicke’s encephalopathy.

A

The presence of neurological symptoms caused by biochemical lesions of the central nervous system following exhaustion of vitamin B (particularly thiamine) reserves.

121
Q

What are the causes of Wernicke’s encephalopathy?

A

o Main cause is chronic alcohol consumption resulting in thiamine deficiency due to inadequate nutritional thiamine intake -> decreased thiamine absorption -> impaired thiamine utilisation by cells

o Other conditions that cause thiamine deficiency = chronic subdural haematoma, AIDS, hyperemesis gravidarum, thyrotoxicosis

o Thiamine deficiency results in abnormal cellular function in the cerebral cortex, hypothalamus and cerebellum

122
Q

What are the presenting symptoms of Wernicke’s encephalopathy?

A

Vision changes = diplopia, eye movement abnormalities, ptosis

Loss of muscle coordination: unsteady gait

Loss of memory

Inability to form new memories

Hallucinations

123
Q

What are the signs of Wernicke’s encephalopathy on examination?

A

o Wernicke’s is classically defined by a triad of signs = confusion, ophthalmoplegia, ataxia

o The patient is usually mentally alert with vocabulary, comprehension, motor skills, social habits and naming ability maintained

o Some show signs suggestive of polyneuropathy

o Reflexes may be decreased

o Abnormal gait and coordination

o Eye abnormalities on movement = nystagmus, bilateral lateral rectus palsy, conjugate gaze palsy

o Low temperature

o Rapid pulse

o Some may be cachectic

124
Q

What is Korsakoff’s psychosis?

A

Occurs when the Wernicke’s encephalopathy deteriorates further, leading to the additional symptoms of - amnesia, confabulation

125
Q

What are the appropriate investigations for Wernicke’s encephalopathy?

A

o Diagnosis is mainly based on history and examination

o Possible useful tests = FBC (high MCV is a common feature amongst alcoholics), U&Es (exclude metabolic imbalances as a cause of confusion), LFTs, glucose, ABG (hypercapnia and hypoxia can cause confusion), serum thiamine

o CT head scan may be useful

126
Q

What is Frontotemporal dementia?

A

Specific degeneration of the frontal and temporal lobes.

127
Q

What are the indications for lumbar punctures?

A

o Diagnostic

  • Infectious = Meningitis, encephalitis
  • Inflammatory = MS, Gullain-Barre syndrome
  • Oncological
  • Metabolic
  • Spontaneous subarachnoid haemorrhage

o Therapeutic = Analgesia, Anaesthesia, Antibiotics, Antineoplastics

128
Q

What are the possible complications of a lumbar puncture?

A

o Herniation

o Cardiorespiratory compromise

o Pain

o Headache

o Bleeding

o Infection

o Subarachnoid epidermal cyst

o CSF leakage

129
Q

What are the possible complications of TIA’s?

A

o Recurrence

o Stroke

130
Q

What is hthe major possible complication of regular headaches?

A

o Drug-overuse headaches

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