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1st and 2nd year main conditions > neurological_conditions_20180310144626 > Flashcards

neurological_conditions_20180310144626 Flashcards

1
Q

Aetiologies?

A

IdiopathicAssociated with disease of the thymus

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2
Q

Pathology?

A

Autoantibodies vs AchR at NMJ Leads to failure of muscles to contract and relax properly

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3
Q

Symptoms and signs?

A

Muscle weakness increasing with activity, begins with extraocular and descends with timePtosis, peek sign, snarl, mastication weakness –> dysarthria, dyspnoea, limb weakness and fatigueNO LOSS OF REFLEXES Symptoms worsen during stress and over treatment

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4
Q

Investigations and findings?

A

Tensilon test - diagnostic Autoantibodies - positive EMGCT chest - may reveal thyme disease

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5
Q

Management?

A

Anticholinesterases Immunosuppression Thymectomy if associated thymus disease

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6
Q

Epidemiology?

A

More common in males over 50 and women under 50

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7
Q

Aetiologies?

A

Post infective disease Causitive organisms: Camylobacter jejuni, EBV, Mycoplasma pneumonia

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8
Q

Pathology?

A

Autoantibodies vs infective agents also acting on myelin sheath Leads to acute demyelinating polyneuropathy

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9
Q

Signs and Symptoms?

A

Bilateral ascending muscle weaknessPain Reduced/absent reflexesSensory lossAutonomic signs Respiratory distress

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10
Q

Investigations and Findings?

A

Nerve conduction study - slow conductionLumbar puncture - high protein in CSF

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11
Q

Management?

A

Resuscitation IV immunoglobulin Plasma exchange

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12
Q

Complications?

A

Permanent paralysis in ~10%

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13
Q

Epidemiology?

A

More common in males 15-30 and 50-75

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14
Q

Aetiologies?

A

IdiopathicViralFamilial

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15
Q

Pathology?

A

Progressive destruction of the UMN and LMN in the motor cortex, spinal cord and peripheral nerves

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16
Q

Signs and symptoms?

A

Four main patterns:ALS - lateral cortocospinal tract and anterior horn signsHand small muscle wastingBulbar/psuedobulbar palsies Primary lateral sclerosis - purely UMN signs

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17
Q

Investigations and findings?

A

Careful history and examination MRI excludatory

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18
Q

Management?

A

Palliative - MDT basedSodium channel blocker prolongs life slightly

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19
Q

Complications?

A

Prognosis bleak

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20
Q

Epidemiology?

A

M > F, 3:2

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21
Q

Aetiologies?

A

TraumaNeoplasiaIschaemia Degenerative diseaseDemyelinating diseaseInfection

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22
Q

Pathology?

A

Partial/full hemisection causing a combination dorsal column, spinothalamic tract and corticospinal tract lesions

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23
Q

Signs and symptoms?

A

Ipsilateral UMN signs in lower sectionsIpsilateral proprioception/vibration loss in lower sections Contralateral pain/temperature loss

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24
Q

Investigations and Findings?

A

MRI/CT - will show area and extent of trauma, ischaemia, neoplasia

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25
Q

Management?

A

Treatment of infection if applicable Removal of causative agent if applicable

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26
Q

Aetiologies?

A

Risk factors - cardiovascular disease risk factors

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27
Q

Pathology?

A

Ischaemia of spinal cord portion due to occlusion of a supplying blood vessel

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28
Q

Signs and symptoms?

A

Anything spinal cord related, depends on area of lossUMN signsSensory lossSphincter tone loss

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29
Q

Investigations and Findings?

A

MRI can diagnose - areas of ischaemia seen

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30
Q

Management?

A

Early management vital Surgical repair is an option

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31
Q

Complications?

A

Many will not recover

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32
Q

Aetiologies?

A

Dietary deficiency or lack of gastric intrinsic factor

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33
Q

Pathology?

A

Demyelination

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34
Q

Signs and symptoms?

A

Insidious onset where symptoms begin peripherally and move centrally Spinal cord involvement indicated by UMN signs

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35
Q

Investigations and Findings?

A

B12 serum tests - deficient Intrinsic factor - deficient

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36
Q

Management?

A

B12 supplementation

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37
Q

Aetiologies?

A

Maternal folic acid deficiency

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38
Q

Pathology?

A

Failure of neural tube to fuse during embryogenesis –> spaces in vertebral column

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39
Q

Signs and symptoms?

A

Varying degrees from asymptomatic to complete paralysis Depends on how much of the spinal cord and its coverings protrude through

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40
Q

Investigations and Findings?

A

Severe disease obvious on physical examination Oculta seen incidentally on x-ray later in life Cyst on the back in the midline

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41
Q

Management?

A

Surgical repair ASAP

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42
Q

Complications?

A

Treatment not always successful Quality of life impaired

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43
Q

Aetiologies?

A

Part of MSRarely - sinusitus and other infections

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44
Q

Pathology?

A

Inflammation of the optic nerve +/- optic disc

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45
Q

Signs and symptoms?

A

Visual and colour vision loss Optic pain

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46
Q

Investigations and Findings?

A

Ophthalmoscopy Test for MS

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47
Q

Management?

A

Refer to specialist Corticosteroids

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48
Q

Complications?

A

Progression into MS

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49
Q

Aetiologies?

A

TraumaInfectionInfarctionTumourDiabetic neuropathy Aneurysm Raised ICP

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50
Q

Pathology?

A

Compression or section of the ophthalmic nerve

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51
Q

Signs and Symptoms?

A

Permanent dilatation of eyePainless loss of adduction, extortion and elevation Ptosis

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52
Q

Investigations?

A

Examination

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53
Q

Aetiologies?

A

TraumaInfectionTumourInfarctionDiabetic NeuropathyAneurysmRaised ICP

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54
Q

Pathology?

A

Compression/section of trochlear nerve

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55
Q

Signs and symptoms?

A

Difficulty depressing eyeDiplopia once eye depressed

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56
Q

Investigations?

A

Examination

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57
Q

Aetiologies?

A

TraumaInfectionInfarctionTumourDiabetic NeuropathyAneurysmRaised ICP

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58
Q

Pathology?

A

Compression or section of abducens nerve

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59
Q

Signs and Symptoms?

A

Inability to abduct eye

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60
Q

Investigation?

A

Examination

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61
Q

Aetiologies?

A

TumourInfectionTraumaInfarction MS

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62
Q

Pathology?

A

Demyelination or compression from adjacent structures of trigeminal nerve

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63
Q

Signs and Symptoms?

A

Unilateral sharp, severe bursts of pain in face after a certain trigger

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64
Q

Investigations?

A

History and examination

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65
Q

Management?

A

Carbemazepine Analgesics don’t work

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66
Q

Aetiologies?

A

Trauma InfectionTumourInfarction

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67
Q

Pathology?

A

Compression/section of trigeminal nerve or its branches

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68
Q

Signs and Symptoms?

A

Sensory loss in one or more of the six areas in the face Trouble chewing if UMNLMN causes flaccid paralysis of the affected side of the jaw –> deviation

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69
Q

Investigations?

A

Examination

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70
Q

Aetiologies?

A

MNDGuillean - Barre syndrome PolioMyasthenia gravis Brainstem tumours

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71
Q

Pathology?

A

Damage to the CN IX-XII nuclei which causes impairment to the innervation of the bulbar targets LMN lesion

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72
Q

Signs and Symptoms?

A

LMN signs of the tongue and the muscles of talking and swallowing Tongue fasciculation, jaw jerk absence Quiet/hoarse/nasal speech

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73
Q

Investigations?

A

Examination

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74
Q

Aetiologies?

A

Stroke MNDMS

75
Q

Pathology?

A

Damage to the CN IX - XII which causes impairment to the innervation of the bulbar targets UMN lesionBilateral lesion

76
Q

Signs and Symptoms?

A

UMN signs of swallowing/talking muscles: slow tongue movements, slow speech, hyperreflexia, emotional incontinence

77
Q

Investigations?

A

Examination

78
Q

Aetiologies?

A

Autoimmune with unknown triggerViral MS

79
Q

Pathology?

A

qAutoimmune inflammation of myelin sheath surrounding nerves causing demyelination Resolving of the lesions incomplete –> scarring Axonal loss in later disease

80
Q

Signs and symptoms?

A

Common presentation = relapsing symptoms, sensory signs (dysaethesia, optic neuritis, trigeminal neuralgia), UMN signs, GU signs (erectile, urinary), cognitive signs (amnesia, moodiness) Rarer pattern = as above with progressive worsening, no relapse

81
Q

Investigations and Findings?

A

MRI scan - lesions show up as white plaques, axonal loss as black holes Lumbar Puncture - CSF oligoclonal bands

82
Q

Management?

A

No cure Immunosuppressants can lessen severity of relapses Biologics lessen frequency, Monoclonal abs prevent BBB crossingMDT based

83
Q

Complications?

A

Wheelchair bound Life expectancy is reduced

84
Q

Aetiologies?

A

Environmental and genetic causesRF: strong FH, down syndrome, Vascular RF, alcoholism, smoking

85
Q

Pathology?

A

Selective neuronal loss in the cortex

86
Q

Signs and Symptoms?

A

Main initial domains of neuronal loss: spatial awareness, self awareness, memory, higher function, verbal Progresses into intellect/behavioural/psychotic decline

87
Q

Investigations and Findings?

A

Diagnosis purely clinicalExcludatory investigations

88
Q

Management?

A

No definitive cureMDT based support for family and patient Acetylcholinesterase inhibitors = symptomatic, BP control

89
Q

Complications?

A

Progressive decline into sedation

90
Q

Aetiologies?

A

Associated with parkinson’s

91
Q

Pathology?

A

Lewy body deposits on the brainstem and neocortex resulting in degeneration of neurons

92
Q

Signs and Symptoms?

A

As Alzheimer’s but with fluctuating rather than progressive patternAlso vivid hallucinations

93
Q

Investigations?

A

Diagnosis purely clinicalExcludatory investigations

94
Q

Management?

A

No definitive cureMDT based supportAcetylcholinesterase inhibitors - symptomatic, BP control

95
Q

Complications?

A

Often progresses into Parkinson’s disease

96
Q

Aetiologies?

A

Risk factors = cardiovascular disease risk factors

97
Q

Pathology?

A

Infarction of brain tissue due to occlusion of blood vesselsUsually a build up of many small infarcts

98
Q

Signs and Symptoms?

A

As A.D. but with the addition of a higher likelihood of other focal neurological signs

99
Q

Investigations and findings?

A

Diagnosis purely clinicalExcludatory investigationsInfarctions can be seen

100
Q

Management?

A

No definitive cure MDT supportAcetylcholinesterase inhibitors = symptomatic, BP control

101
Q

Complications?

A

Other forms of atheromatous disease

102
Q

Aetiologies?

A

IdiopathicDrug-inducedVascular Traumatic

103
Q

Pathology?

A

Degeneration of substantia niagra in basal ganglia –> loss of excitatory dopamine in striatum

104
Q

Signs and Symptoms?

A

Parkinsonism triad: pill-rolling tremor, rigidity and bradykinesia Additional features: shuffling gait, loss of facial tone, postural difficulties PD defined as 2 or more of parkinsonism without any focal signs

105
Q

Investigations and Findings?

A

Diagnosis purely clinical Investigations exist but too expensive for routine use

106
Q

Management?

A

Levodopa but last resort Deep brain stimulation

107
Q

Complications?

A

Progressive decline into sedentation

108
Q

Aetiologies?

A

Focal lesionsInfectionsHypoxiaIdiopathic Trauma

109
Q

Pathology?

A

Generalised - bilateral abnormal brain neuron firing showing general manifestations Focal - as above but only focal signs

110
Q

Signs and symptoms of absence seizures?

A

Patient will cease activity randomly and stare blankly Skin pallor, twitchingActivity begins where it left off

111
Q

Signs and symptoms of tonic-clonic seizures?

A

Tonic phase = rigidity, falls, bitten tongue, incontinence Clonic phase = convulsions, frothing of mouth, rhythmic jerking

112
Q

Investigations and Findings?

A

EEGECGCT scanSerum calcium GlucoseCan exclude epilepsy in many cases

113
Q

Management for absence seizure?

A

Sodium valproate Lomotrigine

114
Q

Management for tonic - clonic seizures?

A

Sodium valproate Carbemazepine

115
Q

Complications of absence seizures?

A

Can progress into tonic clonic epilepsy

116
Q

Complications of tonic-clonic epilepsy?

A

TraumaRoad traffic accidents loss of driving licence Status epilepticus

117
Q

Aetiologies of status epilepticus?

A

Anyone with epilepsy can have this type of seizure First presentation as SE is almost unheard of

118
Q

Pathology of status epilepticus?

A

a seizure which lasts more than 30 mins or 2+ seizures in a row without recovery

119
Q

Investigations for status epilepticus?

A

ABG Blood glucoseECG

120
Q

Management of status epilepticus?

A

Secure airway IV/IR diazepam +/- phenytoin if symptoms persist Treat after 5 mins

121
Q

Complications of status epilepticus?

A

10% mortality

122
Q

Aetiologies?

A

Infective - meningococcal, pneumococcalInflammatory Drug induced Malignant

123
Q

Pathology?

A

Infection enters through cranial cavity openings Acute bacterial causes meningeal congestion with neutrophils –> pus Chronic is green exudate with adhesions Viral = lymphocytic inflammation

124
Q

Signs and Symptoms?

A

Meningism = stiff neck, fever, headache, kerning’s sign, photophobiaOthers = pleuritic pain, petechial rash, focal signs, shock, AMS, seizures

125
Q

Investigations and findings?

A

CT - contra/indicat. LPLumbar puncture - CSF findings high protein, high neutrophils, high pressureSerologyBlood culture FBC, U+Es LFT Glucose - hypoglycaemia Coag

126
Q

Management?

A

ABCDIV antibiotics (cephalosporin)Antivirals ITU admission

127
Q

Complications?

A

DeathReduced life expectancyFNS

128
Q

Aetiologies?

A

Infective (viral - HSV, coxsackle. Bac - TB, mycoplasma, listeria) Inflammatory Metabolic Malignant

129
Q

Pathology?

A

Inflammation of the brain parenchyma

130
Q

Signs and symptoms?

A

Classic triad - fever, AMS and headache Others - shock, seizures, focal signs, raised ICP signs

131
Q

Investigations and Findings?

A

CT - contra/indicat. LPLumbar puncture - CSF findings normal/high protein. high lymphocyte SerologyBlood culture FBC, U+Es, LFTs Glucose - normal CoagEEG

132
Q

Management?

A

ABCDIV antibioticsAciclovir Symptomatic treatment

133
Q

Complications?

A

Death Reduced life expectancy FNS

134
Q

Aetiologies?

A

TumourCystHaemorrhage Meningitis/encephalitis HydrocephalusDiffuse brain swelling

135
Q

Pathology?

A

Pressure intracranially increases due to an increased volume of substance in the closed space of the cranium

136
Q

Signs and Symptoms?

A

Headache, visual loss, nausea and vomiting Decreased GCS, cognitive decline, papilloedema, CN palsies, tonsillar compression

137
Q

Investigations and Findings?

A

Not lumbar puncture CT scan indicated

138
Q

Management?

A

Treatment of cause Neurosurgery

139
Q

Complications?

A

Decompensation => tonsillar herniation

140
Q

Aetiologies?

A

AffluencyIonising radiationImmunosuppression Genetic predisposition

141
Q

Pathology?

A

Pathological types = glioblastoma (IV), glioma (I-III), meningioma (I), metastases (I-IV)Symptoms usually correlate with increased ICP due to space occupying lesion

142
Q

Signs and Symptoms?

A

Raised ICPSeizuresFocal neurological signs

143
Q

Investigations and Findings?

A

CT/MRI/PET brain - brain lesions, mets Imaging of other body for metastases/sourceBiopsies of regional lymph nodes

144
Q

Management?

A

Palliation is only option in high grade tumoursAnti-epilepticsAnti-emetics Neurosurgery

145
Q

Complications?

A

Metastases Death

146
Q

Aetiologies?

A

Blockage at any point of the CSF circulation or overproduction of CSF Tumour Raised ICPPost meningitis Normal pressure hydrocephalus

147
Q

Pathology?

A

Build up of CSF in ventricular system which can be obstructive or communicating

148
Q

Signs and symptoms in infants?

A

Enlarged headBulging fontanelles Splayed sutures Sunsetting eyesFTTHigh pitched cry

149
Q

Signs and symptoms in > 18 months?

A

No enlarged headSigns of raised ICP

150
Q

Management?

A

Treat cause of obstructionShunts Endoscopic third ventriculostomy

151
Q

Complications

A

A potentially treatable cause of dementia

152
Q

Modifiable risk factors?

A

HypertensionSmokingDMHyperlipidaemiaAlcoholism Oestrogen based contraception

153
Q

Non-modifiable risk factors?

A

Previous TIA/strokeOld age Being male FH of stroke IHDMalignancy Genetic hypercoagubility Vascular malformations

154
Q

Pathology?

A

Can be occlusive or haemorrhagic Occlusive - infarct blocks blood supply to an area of the brain –> an ischaemic core and penumbra of tissue –> loss of function Haemorrhage - bleed –> tissue damage from blood infiltration and high pressure –> encapsulation in fibrous and glial tissue

155
Q

Signs and symptoms of an anterior cerebral artery stroke?

A

Contralateral UMN signs and corticosensory lossBehaviour abnormalities Dominant speech difficulties or non-dominant hemineglect

156
Q

Signs and symptoms of a middle cerebral artery stroke?

A

Controlalateral face UMN weakness and corticosensory lossBehaviour abnormalities Hemiparesis

157
Q

Signs and Symptoms of a posterior cerebral artery stroke?

A

Vital function loss contralateral hemiparesis Hemisensory loss

158
Q

Signs and symptoms of a lacunar artery stroke?

A

Non cortical: either purely motor or purely sensory DysarthriaHemiparesis

159
Q

Investigation and Findings?

A

Urgent CT/MRI brain scanFBCBiochemU+Es Blood pressure

160
Q

Management?

A

ABCD RecussAssess pros and cons of thrombolysis Anticoagulants when haemorrhage excluded

161
Q

Complications?

A

Lifetime focal symptoms ComaDeath

162
Q

Aetiologies of tension type headache?

A

Triggers include stress, noise, prolonged concentration, anxiety, depression, refractive errors, analgesic overuse, hypertension

163
Q

Aetiologies of migraine?

A

Hypersensitivity to triggers: stress, hormones, hunger, food cravings, sleep disturbance, dehydration, environmental stimuli

164
Q

Aetiologies of Cluster headache?

165
Q

Aetiologies of SUNCT?

A

SporadicTriggers: wind, touch, cold

166
Q

Aetiologies of thunderclap headache?

A

Primary headachesSAHTIA/stroke ICHVertebral artery dissection Meningitis

167
Q

Aetiologies of Giant cell arteritis?

A

Unknown cause

168
Q

Pathology of tension type headache?

A

Generated by neuromuscular irritation with pain referred to scalp

169
Q

Pathology of migraine?

A

Complex changes in brain which hypersensitive the trigeminal ganglion

170
Q

Pathology of cluster headache?

A

Hyperactivity of the trigeminal autonomic systems due to usually unsinister stimuli

171
Q

Pathology of giant cell arteritis?

A

Inflammation of the large arteries in the brain resulting in granulomatous deposits

172
Q

Signs and symptoms of tension type headache?

A

Tight band sensationPressure behind the eyesThrobbing sensation

173
Q

Signs and symptoms of migraine?

A

Prodrome - mood change, yawningAura - Visual cascade, motor dysarthria Headache - very severe, photophobia, phonophobia, nausea and vomiting

174
Q

Signs and symptoms of cluster headache?

A

Excruciating, unilateral pain in bouts lasting months but then remitting for months Associated with orbital/temporal pain, lacrimation, ptosis Pain ceases rapidly

175
Q

Signs and symptoms of SUNCT?

A

As cluster headache but with 10s-4min duration up to 200 times a day Associated symptoms include - conjunctival injection and lacrimation

176
Q

Signs and symptoms of thunderclap headache?

A

Highly intense headache with sudden onset which reaches maximum within 1 minSettles instantaneously

177
Q

Signs and symptoms of giant cell arteritis?

A

Diffuse headache Systemic unwellJaw claudication Visual disturbance Beaded temporal artery

178
Q

Investigation and findings of headaches?

A

If suspicious presentation admit for an MRI/CT brain

179
Q

Investigation and findings of giant cell arteritis?

A

FBC - CRP and ESR elevated, high platelets BiochemU+Es

180
Q

Management of migraine?

A

TriptansNSAIDs Prophylaxis

181
Q

Management of cluster headache

A

100% O2 Triptans Short course steroids

182
Q

Management of SUNCT?

A

Symptomatic reliefAnalgesics Anti epileptics

183
Q

Management of thunderclap headache?

A

Treat cause

184
Q

Management of giant cell arteritis?

A

High dose prednisolone

1st and 2nd year main conditions (27 decks)

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