Neuro 5 Flashcards
What are the ischaemic causes of stroke?
Large artery atherosclerosis Cardioembolic Small artery occlusion Undetermined Rare causes - arterial dissection, venous sinus thrombosis
What are the haemorrhagic causes of stroke?
Primary intracerebral haemorrhage
Secondary haemorrhage
>Subarachnoid haem
>Arteriovenous malformation
How are lipid levels related to stroke?
An increase in serum lipids levels leads to an increase in plasma level of LDL
Resulting in greater amounts of LDL in arterial wall and atheroma
HT, cigarette + diabetes all contribute
What are the symptoms of ACA occlusion?
Contralateral:
>Paralysis of foot/leg
>Sensory loss over foot/leg
>Impairment of gait/stance
What are the symptoms of MCA occlusion?
Contralateral: >Paralysis of face/arm/leg >Sensory loss face/arm/leg >Homonygmous heminaopia >Gaze paralysis contralateral Aphasia if on dominant (left) side Unilateral neglect and agnosia if non dominant stroke (norm right)
What are the symptoms of a left hemisphere stroke?
Left Hemiplegia,
Left homonymous hemianopia,
dysphasia
What are the symptoms of a Right hemisphere stroke?
Left hemiplegia, homonymous hemianopia
Neglect syndromes
Visual, sensory agnosia, anosagnosia (denial of hemiplegia), prosopagnosia (failure to recognise faces)
What are the lacunar stroke symptoms?
Devoid of cortical signs
Pure motor or sensory stroke
Dysarthria (clumsy hands)
Ataxic hemiparesis
What are the posterior circulation stroke symptoms?
Brain stem, cerebellum, thalamus, occipital + medial temporal lobes affected
Coma, vertigo, nausea, vomiting, cranial nerve palsies, ataxia
Hemiparesis, hemisensory loss
Crossed sensorimotor defcits
Visual field deficits
What are the criteria for TPA use?
Less than 4.5 hours since onset
Disabling neurological deficit
Symptoms present for greater than 60mins
Consent is obtained
What are teh exclusions for TPA use?
Anything increasing possibility of haemorrhage >Blood on CT >Recent surgery >Recent episodes of bleeding >Coagulation problems BP > 185 systolic, >110 diastolic Glucose <2.8 or > 22
What is the secondary prevention for stroke?
Antihypertensives Antipolateltes Lipid lowering agents Warfarin for AF Carotid endartectomy
What are differentials to stroke?
Posti-ictal states Hypoglycaemia Intracranial masses Vestibular disease Bell's palsy Functional hemiparesis Migraine Demented patients with UTIs
What is dementia?
Progressive impairment of multiple domains of cognitive function in alert patient leading to loss of acquired skills and interferences in occupational and social role
Common and increasing prevalence, incidence 200/100000
What are the causes of late onset dementia?
Alzheimers 55%
Vascular 20%
Lwey body 20%
Other 5%
What are the causes of early onset dementia?
Alzheimers 33% Vascular 15% Frontotemporal 15% Other 33% >Toxic (Alcohol), >genetic (huntingtons), >infection (HIV, CJD), >inflammatory (MS)
What is late onset dementia vs early dementia?
Late onset is after 65 years old
Early onset any time before that
What are the treatable causes of MS?
Vitamin deficiency - B12
Endocrine - thyroid disease
Infective - HIV, syphilis
How do you diagnose dementia?
History (independent witness) - type of deficit, progression, FH, risk factors
Exam - cognitive function, neurological, vascular
Investigations - routine bloods, CT/MRI
Others - CSF, EEG, functional imaging, genetics
How do you examine cognitive function?
Various domains - memory, attention, language, visuo-spatial, behaviour, emotion, executive function apraxias, agnosias
Screening tests - mini-mental (MMSE), Montréal (MOCA)
Neuropsychological assessment
What are the indicators for specific types of dementia?
type of cognitive deficit speed of progression >rapid progression (CJD) >stepwise progression (vascular) other neurological signs >abnormal movements (Huntington's) >parkinsonism (Lewy body) >Myoclonus (CJD)
What are the types of alzheimers disease?
Tempo parietal dementia
frontotemporal dementia
What is tempoparietal dementia?
early memory disturbance
language and visuospatial problems
personality preserved until later
What is frontemporal dementia?
early change in personality/behaviour
often changing eating habits
early dysphasia
memory/visuospatial relatively preserved
What are the non-pharmacological treatments for dementia?
information support
Occupational Therapy
social work/support/respite/placement
voluntary organisations
What are the pharmacological treatments for
Alzheimer’s disease?
Cholinesterase inhibitors (cholinergic deficit) NMDA antagonist (memantine)
What are the examples of cholinesterase inhibitors?
Donepezil, rivastigmine, galantamine
Name an NMDA inhibitor.
memantine
What is parkinsonism?
Bradykinesia rigidity tremor postural instability pathology in basal ganglia – predominately dopamine loss
What are the types of Parkinson’s disease?
idiopathic,
drug induced (dopamine antagonist),
vascular Parkinson,
Parkinson’s plus syndromes (multiple system atrophy, progressive supra-nuclear policy
How do you diagnose Parkinson’s?
Bradykinesia plus one or more of
>tremor rigidity
>postural instability
no other cause
slowly progressive
supported by asymmetric rest tremor, good response to deepening replacement
What are the complications of Parkinson’s? (Drugs)
motor fluctuations – levodopa wears off
dyskinesia’s – in voluntary movements
psychiatric – hallucinations, impulse control
What are the non-drug complications of Parkinson’s?
depression dementia autonomic (BP, bladder, bowel) speech, Swallow balance
How do you treat Parkinson’s?
prolong levodopa half life
>MAOB inhibitors,
>COMT inhibitor, slow-release)
add dopamine agonist continuous infusion (Apomorphine, Duodopa) functional neurosurgery (deep brain stimulation) Allied health professionals
What is the choroid plexus responsible for, where is it found?
Responsible for production of CSF
Mostly floor of lateral ventricles
Some in roof of 3rd/4th
What is the flow pathway for CSF?
Lateral ventricles Foramina of Munro 3rd Ventricle Aqueduct of Sylvius 4th Ventricle Foramen of Magendie (medial, x1) & Foramen of Luschka (lateral, x2) Subarachnoid spaces Arachnoid granulations Dural venous sinuses
What are teh clasifications of hydrocephalus?
Obstructive - blockage of flow from ventricles
Communicating - block at level of arachnoid granulations
What are the congenital causes of hydrocephalus?
Chiari malformation
Aqueductal stenosis
dandy walker malformation
What are the acquired cases of hydrocephalus?
meningitis post haemorrhagic neoplastic Post op Cerebellar stoke post-traumatic
What are the clinical features of hydrocephalus in infants?
Cranial enlargement – regular measurements of circumference needed Splaying of cranial sutures Irritable, poor feeding Fontanelles full & bulging Engorged scalp veins Abducens (VI nerve) palsy Perinaud’s syndrome: ‘sunsetting’ (upward gaze palsy) Convergent nystagmus Eyelid retraction Exaggerated reflexes Respiratory problems
What are the clinical features of hydrocephalus in adults and children?
Increased ICP Headaches >worse in the morning, worse on cough/ straining Papilloedema Visual disturbances Gait abnormality Loss of upgaze or abducens palsy Impaired consciousness
What is the medical treatment of hydrocephalus?
may help as a temporising measure
Acetazolamide (carbonic anhydrase inhibitor)
>Reduces CSF production from choroid plexus
What are the surgical measures for managing hydrocephalus?
In emergency situation – EVD (external ventricular drain) Eliminating obstruction CSF diversion >3rd Ventriculostomy >Shunt insertion
What are the possible complications of shunts?
Over-drainage >low pressure headaches, >subdural haematoma Under-drainage Blockage Infection Disconnection Seizures Distal end problems: >Abdominal hernias (VPS) >Cardiac arrhythmias (VAS)
What is ETV?
Endoscopic 3rd ventriculostomy (ETV)
Creating a fistula between 3rd ventricle and subarachnoid spaces / basal cisterns
Only works for non-communicating hydrocephalus
What is normal pressure hydrocephalus?
A potentially reversible dementia Classical triad >Dementia >Gait disturbance (magnetic gait) >Urinary incontinence Age >60
‘Normal’ pressure on LP – diagnostic challenge
Improvement after shunt
What is idiopathic hydrocephalus?
BIH / pseudotumour cerebri Raised ICP without obvious cause Typical patient is young obese female Often present with headaches & visual disturbances – papilloedema Patients will go blind without treatment
How do you treat idiopathic hydrocephalus?
Lose weight!! (need to lose 6%)
Medical - acetazolamide
CSF diversion – VP or LP shunt
Optic nerve sheath fenestration
What are the indications for lumbar puncture?
Obtain CSF for analysis
>Rule out bacterial or viral infection
>Measure for blood breakdown products (SAH)
>Measure protein load
>Test for the weird and wonderful
Measurement of pressure (intracranial pressure (ICP))
CSF drainage for raised pressure
Diagnostic test for Normal Pressure Hydrocephalus
What are the risks of lumbar puncture?
Bleeding Infection Nerve root injury Retroperitoneal / intra-abdominal injury Brainstem herniation
What is the CSF like in meningitis?
Cloudy, turbid
WBC - lots!! – mostly polymorphs
Protein >1g/l
Glucose - low
What causes CSF to be yellow?
Xanthochromic >Yellow due to blood breakdown products >Most commonly seen in SAH >In patients with suspected SAH based on history – with a normal CT scan – CSF spectrophotometry used to detect blood breakdown products (bilirubin) >>Positive only after 12hrs >>Persists for 3 weeks
What are the types of dopaminergic drugs?
Dopamine precursor
Dopamine agonists
What are examples of dopamine precursors?
Levodopa
What are the examples of dopamine agonists?
Bromocriptine, pergolide
Ropinirole
Pramiexole
Apomorphine
What eznyme inhibtors are useful in Parkinson’s?
Peripheral AAAD inhibitors
MOAB, COMT inhibitors
What are peripheral AAAD inhibitors?
benserazide
Reduce peripheral side-effects of levodopa, allowing greater amount to reach CNS
What are MOAB/COMT inhibtors?
MOAB - selegine
COMT - entacapone
Reduce metabolism of dopamine and so increase effectiveness of levodopa
How do dopaminergic drugs affect Parkinson’s?
Improve parkinsons (rigidity + bradykinesia)
Fail to help “midline” features (dysathria, balance, cognition)
Worsen or cuse (Nausea, vomiting, psychosis)
How do dopamine antagonists affect parkinson’s?
Improve (nausea, vomiting, psychosis)
Worsen/cause parkinsons (rigidity + bradykinesia)
What is domperidone?
Dopamine antagonist that doesn’t cross the blood-brain barrier
Antiemetic
No antipsychotic properties
Relatively safe in PD
Has permitted therapeutic use of apomorphine
What drugs can cause dyskinesias?
Dopaminergic drugs (may cause dyskinesias - eg chorea) DA antagonists - may cause parkinsonism
What is hypocondriasis?
Preoccupation with disease + fear of illness
Persistent belief od unidentified disease
Requests for repeated reassurance/investigation
What is somatisation disorder?
Example of abnormal illness behaviour
Chronic, onset before 30
Multiple unexplained physical symptoms
What is conversion disorder?
“hysteria”
Loss of function of a body part
Signs mimic neurological disease + inconsistent
Patient not conscious of mechanisms, information from functional imaging
What is malingering?
Inconsistent signs, may mimic neurological disease
Patient conscious of mechanisms
What is chronic fatigue syndrome?
Chronic
Multiple physical symptoms - fatigue, arthralgia, myalgia
May overlap with other syndromes - eg fibromyalgia, chronic pain
Worse after exertion
What is non-epileptic attack disorder?
Attacks look like epilepsy but not caused by abnormal electrical activity in the brain
Drug resistant
Abuse or neglect in childhood risk factor
Associated with anxiety, depression and post traumatic stress disorders
How do you manage unexplained symptoms?
Exclude physical disease Carry out essential investigations, ovoid repeated ones Psychiatric assessment Explanations to patient Consider anti-depressants Consider cognitive behaviour therapy.
What is post traumatic amnesia?
Period of recovery following traumatic brain injury
Disorientation - unable to locate themselves in time/space
Anterograde amnesia - inability to remember new events/experiences ocured after brain injury
What should a cognitive function clinical interview entail?
Test memory - new learning in daily life
Language - word finding, errors, poor understanding etc
Processing speed - slowed down, long responses
Attention/concnetration
Executive functioning - difficulty making decisions
Personality - behaviour changes
Insight
Visual spatial - route finding etc
What are the clinical features of spinal cord disease?
Pain - local or referred
Sensory - pins & needles, tingling (paresthesia) and numbness
Proprioception and temperature appreciation
Motor - weakness or complete plegia
Deformity
What does cord compression lead to?
Upper motor features >Weakness >Increased tone >Increased reflexes >Upgoing plantar response >Clonus
What does peripheral nerve root compression lead to?
Lower motor features >Wasting of muscle >Fasciculation >Weakness >Decreased tone >Decreased reflexes >Plantar response - decreased or absent
What are the common causes of degenerative spinal disease?
Cervical spodylosis >Myelopathy, radiculopathy Lumbar spondylosis >Radiculopathy >Cauda equina syndrome Spinal trauma
What is cauda equina syndrome’s triad?
> Bilateral leg pain
Bladder +/1 bowel symptoms
Saddle sensory symptoms
What are the features of carpal tunnel syndrome?
Pain worse at night
Pareatheisa/numbness
Median nerve compressed at wrist resulting in the numbness/pain
What are the sudden onset long term neurological conditions?
Acquired brain injury
Spinal cord injury
Stroke
What are the intermittant causes of long term neurological conditions?
Epilepsy
Early stages of MS
What are the progressive causes of long term neurological diseases?
Motor neurone disease
Parkinsons
Later stages of MS
What are the stable causes of long term neurological conditions?
Post-polio syndrome
Cerebral palsy
Spina bifida
What are some other long term neurological conditions?
Guillain barre syndrome
Muscle diseases
Hereditary spastic paraparesis
Huntingtons
What is spasticity?
Motor disorder characterised by velocity dependent increase in stretch reflexes with exaggerated tendon jerks
Disordered sensoriomotor control resulting from UMN lesion, presenting as intermittent or sustatined inoluntary activation of muscles
What are the complications of spasticity?
Poor seating and lying positions Sleep difficulties and fatigue Dressing and hygiene issues Pain, spasms and associated reactions Communication and feeding problems Pressure sores and contracture Poor self-image and relationship issues
How do you manage spasticity?
Prevention,Prevention and Prevention! Multidisciplinary team approach Physical therapy Exclude exacerbating factors Oral antispasticity agents Focal treatment with Botulinum toxin Drug Treatment not always necessary!
What determines the severity of a head injury?
GCS,
length of loss of consciousness
post-traumatic amnesia are important
