Summary Neurological conditions summaries

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