Summaries of all the neurological conditions as covered in Davidson’s and Oxford Clinical Handbook.
Covers clinical features, key investigations, aetiology, risk factors, and management for all conditions.
Have double checked all management plans with current NICE guidelines
NEUROLOGY SUMMARIES
CONTENTS
Abnormal speech and language
Autoimmune encephalitis
Brain lesions (localisation)
Brain tumours
Degenerative cervical myelopathy
Dementia
Epilepsy
Guillain-Barre syndrome
Idiopathic intracranial hypertension
Idiopathic PD
Migraine
MND + SMA
Movement disorders
Multiple sclerosis
Myaesthenia Gravis
Non-Parkinsonian movement disorders
Other neurological disease
o Acute disseminated encephalomyelitis
o Transverse myelitis
o Neuromyelitis optica
Restless legs
Spinal cord lesions
Status epilepticus
Stroke
Stroke syndromes
Stroke (haemorrhagic)
o Intracerebral haemorrhage
o Subarachnoid haemorrhage
Subdural haemorrhage
TIA
Tension type headache
Trigeminal neuralgia and cluster headaches
Appendix
Drugs causing peripheral neuropathy
Drugs for IPD
,ABNORMAL SPEECH AND LANGUAGE
DYSPHONIA
Reduction in sound/volume – most commonly caused by laryngitis
Neurological causes: lesion of CNX, Parkinsonism can cause hypophonia often in association with dysarthria
DYSARTHRIA
Characterised by poorly articulated or slurred speech
Can occur in association with lesions of the cerebellum, brainstem, and lower cranial nerves, as well as in
myasthenia or myopathic disease
Language function is not affected
DYSPHASIA/APHASIA
Disorder of the language content of speech
Can occur with lesions over a wide area of dominant hemisphere
Categorised as to whether speech is fluent/non-fluent
Fluent or receptive aphasia: impairment mostly related to the input or reception of language, with
difficulties in auditory verbal comprehension or in repetition of words spoken by others. Speech is easy and
fluent but there are difficulties related to the output of language as well, such as paraphasia (substitution of
similar sounding non-words) and neologisms (non-existent words)
Wernicke’s aphasia – localises to the superior posterior temporal lobe: fluent dysphasia with poor
comprehension and poor repetition
o Typically due ischaemia in the posterior superior temporal lobe in the territory of the superior
division of the left middle cerebral artery
Transcortical sensory aphasia: fluent aphasia with poor comprehension and good repetition
o Usually from ischaemia involving the watershed area between the L MCA and L ACA territory
Conduction aphasia: fluent aphasia with good comprehension and poor repetition
o Typically due to ischaemia affecting the inferior parietal lobule
Anomic aphasia – impaired naming
o Tissue damage in the angular gyrus or posterior middle/inferior temporal cortex
Non-fluent or expressive aphasias: difficulties in articulating but relatively good auditory verbal
comprehensive
Broca’s aphasia – associated with pathologies in the inferior frontal region: good comprehension and
poor repetition
o Usually associated with ischaemia or other lesions in the left posterior inferior frontal cortex in
the distribution of the superior division of the left middle cerebral artery
Transcortical motor aphasia – good comprehension and good repetition
Global aphasia – severe impairment in all aspects of language
o Ischaemia often involves both anterior and posterior language areas
MOST COMMON CAUSES OF SPEECH DISTURBANCE
Ischaemic stroke
Intracerebral haemorrhage
Alzheimer’s disease
Traumatic head injury
,AUTO-IMMUNE ENCEPHALITIS
CLINICAL SIGNS
Encephalitis = inflammation of the brain (can be infectious or non-infectious), with autoimmune causes
being increasingly recognised
In general, autoimmune encephalitis does not tend to cause fever or sepsis in the same way as infective
encephalitis
Onset over days to weeks
Patients get gradually worse with fluctuations
High frequency of seizures from onset
CSF WCC usually < 100, usually 100-1000s in infective endocarditis
Mild elevation of CSF proteins
CSF oligoclonal bands: negative, paired, unpaired, polyclonal
MRI: often normal, focal ‘inflammatory’ lesions, enhancement
NMDA-R ENCEPHALITIS
Clinical features
Neuro-psychiatric features: psychosis, delusions, hallucinations, catatonia (waxy flexibility, often very
withdrawn)
Movement disorder – “orofacial dyskinesia” – sticking tongue out, chewing
Seizures
Decreased conscious level “obtunded”
Typical patient: young women, ovarian teratoma common
VOLTAGE GATED POTASSIUM CHANNEL (VGKC) ENCEPHALITIS
Clinical features
Rapid progressive cognitive decline (amnesia)
Focal seizures (facio-brachial dystonic seizures) – brief, often one-handed twitching +/- one-sided
facial twitch
Hyponatraemia
Limbic changes on MRI
Typical patient: Older man, look for cancer (lung or thymoma)
TREATMENT
Supportive: treat seizures, higher level care often required, hard because patients are often psychiatrically
disturbed and may need to be treated in ITU
1st line:
High dose corticosteroids
IVIg
Plasma exchange
2nd line
Rituximab
Cyclophosphamide
, BRAIN LESIONS (LOCALISATION)
PARIETAL LOBE LESIONS OCCIPITAL LOBE
Sensory inattention Homonymous hemianopia (with macula
Apraxias sparing)
Astereognosis (tactile agnosia) Cortical blindness
Inferior homonymous quadrantanopia Visual agnosia
Gerstmann’s syndrome (lesion of the
dominant parietal):
o Alexia
o Acalculi
o Finger agnosia
o R-L disorientation
TEMPORAL LOBE LESIONS FRONTAL LOBE LESIONS
Wernicke’s aphasia – word substitution, Expressive (Broca’s) aphasia: speech is non-
neologisms, but speech remains fluent fluent, laboured, and halting
Superior homonymous quadrantonopia Disinhibition
Auditory agnosia Perseveration
Prosopagnosia (difficulty recognising faces) Anosmia
Inability to generate a list
CEREBELLAR LESIONS
Midlines lesions: gait and truncal ataxia
Hemisphere lesions: intention tremor, past
pointing, dysdiadokinesis, nystagmus
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