Neuro 2 Flashcards
what are the different types of brain tumours
glioma (30%) - astrocytoma, oligodendroglioma, ependymoma
Meningioma - benign but can cause mass effect
pituitary tumours
acoustic neuroma
clinical features of pituitary tumours
bi-temporal hemianopia
hormonal imbalance
clinical features of acoustic neuroma
unilateral hearing loss
tinnitus, balance problems
can be associated with facial nerve palsy
what are some possible tumours that can have mets in the brain?
lung
breast
prostate
colorectal
clinical features of brain tumors
focal neuro signs - depends of the location of tumours
headaches - worse on the morning
raise ICP - papilloedema, altered mental state, visual fields defects, seizures (particularly focal) unilateral ptosis, 3rd and 6th nerve palsies
if frontal lob - personality change, disinhibition
parietal lobe - dysarthria
investigation and management of brain tumours
bloods - coag, blood film for bleeding disorder, hypercalcemia, SIADH - ADH, initial assessment of other possible causes of headaches eg ESR and CRP (elevated in GCA)
CT/MRI scan
PET
biopsy and tumour removal - stereotactic biopsy via skull bur-hole to obtain histology
open exploration (crainotmy) maybe required eg for a symptomatic meningoma
dexamethason - to reduce ICP
- Palliative, chemo, radio, surgery
a complication of a brain tumour
acute haemorrhage into a tumour
bloackage of CSF outflow, causing hydrocephalus
sudden death may occur asa result of obstruction of outflow drainage from 3rd ventricle
sudden inc in ICP = herniation –> high mortaility
definition of encephalitis
inflammation of the brain
aetiology of encephalitis
- Viral infection = main cause of encephalitis, herpes = most common
- bacterial infection can occur Neisseria meningitides = most common
- Viral infection e.g. herpes simplex, VZV, mumps, measles, flu.
- Foreign: Japanese B encephalitis virus, west nile virus, ticks. Sometimes encephalitis can develop with rabies virus infection after an animal bite.
clinical features of encephalitis
high fever headaches muscle aches/weakness or paralysis feeling tired, confused and drowsy N+V beck and back stiffness photophobia change in personality/behaviour hallucinations seizures LOC
IX for encephalitis
bloods - FBC, U&E, CRP, swab tests (if blistering skin rash suspecting herpes simplex)
CT/MRI - alternative causes and check for signs of inc ICP in order to perform LP
LP
EEG
mx for encephalitis
- Supportive- fluids, medicine to control seizures, oxygen, pain and high temperature medication.
- Antiviral medication – acyclovir
- Antibitoics – cefotamine (cover for meningitis)
complications for encephalitis
speech problems weakness and movement disorders swallowing problem seizures chronic headaches personality changes memory problems behavioural problems mood problem, anxiety and depression difficulty concentrating
definition of fibromyalgia
Chronic pain syndrome diagnosed by the presence of widespread body pain
aetiology of fibromyalgia
unknown
CNS - excessive level of pain stimulators or amplifiers in the CNS in response to triggers in the muscles which could not normally cause pain
peripheral and central hyperexcitability in spinal or brainstem level
altered pain perception
risk factor of fibromyalgia
female
30-50 yrs old
clinical features of fibromyalgia
chronic - over 3 months
pain at multiple sites - low back pain with no radiation, neck and shoulder pain are common presentations
morning stiffness
fatigue
sleep disturbances
paresthesia
feeling of swollen joints - no objective swellings
problem with cognition - memory disturbances, difficulty with words finding - fibro fog
headaches, lightheaded or dizzy, fluctuations in weight, anxiety, and depression
Ix for fibromyalgia
bloods - ESR, TFT< ANA - be careful not to over investigate
fibromyalgia questionnaire - used to assess function, it also has a role in review and assessment of treatment interventions
differentials for fibromyalgia
chronic fatigue syndrome hypothyroidism polymyalgia rheumatica inflammatory and metabolic myopathies polymyositis
mx of fibromyalgia
aim = reduce symptoms and improve quality of life not cure
MDT approach
non-drug - aerobic exercise programmes, CBT, acupuncture
drug - WHO analgesic ladder, antidepressants
definition of hydrocephalus
Increase in the volume of CSF occupying the cerebral ventricles. This is usually as a result of impaired absorption, but it may occasionally be due to excessive secretion.
aetiology of hydrocephalus
- Non-communicating/obstructive – flow of CSF obstructed within the ventricles or between the ventricles and the subarachnoid space.
- Communicating- here is communication between the ventricles and the subarachnoid space and the problem lies outside of the ventricular system (eg, due to reduced absorption or blockage of the venous drainage system). It may also be due to increased CSF production.
clinical features of infant hydrocephalus
irritability, vomiting and impaired function
rapid inc in head circumference - HC in 98th centile for he age or greater
the disjunction of sutures dilated scalp veins, tense fontanelle
setting-sun sign - both ocular globes deviate downwards, the upper lids are retracted and the white sclerae maybe visible above the iris
macewen’s sing - a cracked pot sound on percussing the head
inc limb tone
clinical features of older children and adults hydrocephalus
acute onset - headache and vomiting, papilloedema and impaired upwards gaze
gradual onset - unsteady gait due to leg spasticity, large head (although sutures are closed, the skull still enlarges due to chronic inc ICP), unilateral or bilateral 6th nerve palsy.
clinical features of adults hydrocephalus
cognitive deterioration neck pain N+V blurred and double vision incontinence
investigation of hydrocephalus
CT - ventricular enlargement
dilated lateral and 3rd ventricle
with normal 4th ventricle - aqueduct stenosis
with abnor 4th ventricle - fossa mass
generalized ventricular dilation suggesting communicating
US for children - through the anterior fontanelle
differentials for hydrocephalus
brain tumours childhood migraine frontal lobe syndrome epilepsy infection
management of hydrocephalus
surgical is definitive
- external ventricular drain
- ventriculoperitoneal shunt
drugs
- furosemide & acetazolamide inhibits secretion of CSF by the chorotid plexus
- isosorbide promotes reabsorption of CSF
definition of myasthenia gravis
autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest
aetiology of myasthenia gravis
85% due to
- Acetylcholine receptor antibodies bind to the post synaptic membrane at NMJ
- this blocks the receptor preventing acetylcholine stimulant and muscle contraction
- as receptors are used more and more during activity, there is more muscle weakness and more muscle are used
15% due to
- LRP4 and MuSK antibodies – theses are important in the creation and organisation of acetylcholine receptors, destruction of these proteins by autoantibodies also causes symptoms.
what are the 3 antibodies associated with myasthenia gravis?
85% - acetylcholine receptor antibody
15% - LRP4 and MuSK antibodies
what population is most affected by myasthenia gravis
<40 - female
male - > 60
common in those with thyoma (benign tumour of the thymus)
clinical features of myasthenia gravis
severity greatly varies
symptoms best in the morning and worse at end of day
- diplopia
- bilateral ptosis
- weakness in facial movement
- difficulty with swallowing
- fatigue in the jaw when chewing
- slurred speech
- progressive weakness with repetitive movements
what is a myasthenia crisis
acute worsening of symptosm triggered by illness eg RTI
can lead to resp failure as a result of weakness of muscles of respiration
pt require BiPAP, intubation and ventilation
Ix of myasthenia gravis
specific antibody tests - acetylcholine antibodies, muscle-specific kinase antibodies, low-density lipoprotein receptor-related protein 4
CT/MRI thymus
edrophonium test - if diagnostic uncertainty - give IV edrophonium chloride or neostigmine which are acetylcholinesterase inhibitors and temporarily relieves symptoms
mx of myasthenia gravis
reversible acetylcholinesterase inhibitor (pyridostigmine, neostigmine)
- immunosuppression - prednisolone, amabzathioprine
thymectomy
monoclonal antibodies - rituxi
what is the definition of motor neuron disease
an umbrella term that encompasses a variety of specific diagnoses
progressive and fatal condition in which eventually the motor nerves stop functioning
what are the different types of motor neuron diseaes
amyotrophic lateral sclerosis - most common, think Stephen Hawkin
progressive bulbar palsy - affects the muscle of talking and swallowing
progressive muscular atrophy
primary lateral sclerosis
RF for motor neuron disease
hereditary
smoking, pesticides, heavy metals (carcinogens)
clinical features of motor neuron disease
insidious progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech
- often complain of tripping, losing grip, inc fatigue when exercising, slurred speech
lower motor neuron disease
- muscle wasting
- reduced tone
- fasciculations
- reduced reflexes
upper motor neuron disease
- inc tone or spasticity
- brisk reflexes
- upgoing plantar reflexes
- ve Hoffmans sign - cervical myelopathy/MS - flick nail of middle finger, +ve if flexion of the thumb
what are the clinical features of amyotrophic lateral sclerosis
LMN signs in arms
UMN signs in legs
what are the clinical features of primary lateral sclerosis
UMN signs only
what are the clinical features of progressive muscular atrophy
LMN signs only
what are clinical features of bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles
Ix of motor neurone disease
clinical diagnosis
mx of motor neurone disease
no effective treatment of halting or reversing the progression of the disease
riluzole - can help to slow progression and extend survival by few months in ALS
NIV - at night to support breathing
end of life planning is key
what is sinus venous thrombus?
it is when a thrombus form within the cranial venous drainage system causing damages.
most common place for a sinus venous thrombus to occur would be the cavernous sinus which are behind both eyes
what are the important structures within the cavernous sinus
internal carotid arteries
CN: 3, 4, 5, 6
postganglionic sympathetic nerve fibre
aetiology of sinus venous thrombus
local infection - due to nose, sinuses or teeth infection
carotid - cavernous venous fistula - carotid artery dissection in the cavernous sinus
infection in the brain eg meningitis
pituitary adenoma
mets tumours
aneurism of the internal carotid artery within the sinus
clinical features of sinus venous thrombus
acute onset headache unilateral +/- photophobia
ophthalmoplegia +/- diplopia - due to lesion on 3,4,6, usually unilateral but can later progress to both eyes
seizures
other neuro signs - maybe absence, but can include hemiparesis, lower limb weakness, aphasia or ataxia
facial pain - inc pressure
pulsatile proptosis - carotid artery aneurysm
horner’s syndrome - o Post ganglionic sympathetic nerve fibres being affected
investigation for sinus venous thrombus
Often low on the headache differential list.
Bloods – FBC, U+Es, CRP, ESR
LP
Imaging – CT (can miss cases), MRI (do a venogram)
mx for sinus venous thrombus
Refer to neuro.
Consider broad spectrum antibiotics vancomycin + ceftriaxone
(common causes – staph and step.)
anticoagulation – warfarin and heparin
hydrocortisone/dexamethasone to reduce swelling
surgery
clinical features of ataxia
This movement disorder affects the part of the brain that controls coordinated movement (cerebellum). Ataxia may cause uncoordinated or clumsy balance, speech or limb movements, and other symptoms.
clinical features of cervical dystonia
This condition causes long-lasting contractions (spasms) or intermittent contractions of the neck muscles, causing the neck to turn in different ways.
clinical features of chorea
characterized by repetitive, brief, irregular, somewhat rapid, involuntary movements that typically involve the face, mouth, trunk and limbs.
clinical features of dystonia
involves sustained involuntary muscle contractions with twisting, repetitive movements. Dystonia may affect the entire body (generalized dystonia) or one part of the body (focal dystonia).
clinical features of functional movement disorder
may resemble an of the movement disorder but is not due to neurological disease
clinical features of Hungtion’s disease
this is an inherited progressive, neurodegenerative disorder that causes uncontrolled movements (chorea), impaired cognitive abilities and psychiatric conditons
clinical features of multiple system atropy
This uncommon, progressive neurological disorder affects many brain systems. Multiple system atrophy causes a movement disorder, such as ataxia or parkinsonism. It can also cause low blood pressure and impaired bladder function.
clinical features of Parkinson’s Disease
This slowly progressive, neurodegenerative disorder causes tremor, stiffness (rigidity), slow decreased movement (bradykinesia) or imbalance. It may also cause other nonmovement symptoms.
clinical feature of Parkinsonism
a group of conditions that has symptoms similar to those of Parkinson’s Disease
clinical feature of progressive supranuclear palsy
This is a rare neurological disorder that causes problems with walking, balance and eye movements. It may resemble Parkinson’s disease but is a distinct condition.
clinical feature of restless leg syndrome
This movement disorder causes unpleasant, abnormal feelings in the legs while relaxing or lying down, often relieved by movement.
clinical feature of tardive dyskinesia
This neurological condition is caused by long-term use of certain drugs used to treat psychiatric conditions (neuroleptic drugs). Tardive dyskinesia causes repetitive and involuntary movements such as grimacing, eye blinking and other movements.
clinical feature of tourette syndrome
This is a neurological condition that starts between childhood and teenage years and is associated with repetitive movements (motor tics) and vocal sounds (vocal tics).
what is multiple sclerosis
A chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system.
pathophysiology of multiple sclerosis
causes by an inflammatory process involving activation of the immune cells against the myelin.
- Inflammation around myelin and infiltration of immune cells that cause damage to the myelin.
- This affects the way electrical signals travel along the nerve leading to symptoms of MS.
- In early disease remyelination can occur resolving symptoms, in the later stages’ re-myelination is incomplete
- MS affects different nerves at different times.
what are clinical features of MS
charcot’s triad
- dysarthria - difficult or unclear speech due to plagues in brainstem - eating and drinking, swallowing
- nystagmus - optic neritis (central scotoma, pain on eye movement, impaired colour vision, relative afferent pupillary defect), diplopia
- intention tremor - plagues along motor pathways (muscle weakness & spams), ataxia
other signs
- Lhermitte’s sign - electric shock down back and radiates to limbs when bend neck
- +ve hoffman sign - flick nail of middle finger, flexsion of thumb
focal weakness –> bell’s palsy, horner’s syndrome, limb paralysis
plagues in autonomic system
- bowel and bladder symptoms
- sexual dysfunction
higher order activities
- poor concentrations & critical thinking
- depression and anxiety
investigations for multiple sclerosis
• Symptoms must progress over a period of 1-year to diagnose primary progressive MS.
• MRI- typical lesions (white matter plagues)
• Anti-neuromyelitis optica antibody – present in neuromyelitis optica
• Lumbar puncture: oligoclonal bands in CSF.
- visual evoked potential - prolonged
management of multiple sclerosis
• Referral to neurology- they make diagnosis.
• Acute – methylprednisolone +/- plasmapheresis
• Optic neuritis- refer to ophthalmologist: treated with steroids, cyclophosphamide, IVIG, recovery takes 2-6 weeks.
• Plasmaphereisis help to remove any antibodies from blood
• Chronic treatment recombinant beta interferon + symptomatic control
o Fatigue Amantadine/modafinil/ armodafinil
o Urinary frequency oxybutynin
o Pain TCA
o Inc muscle tone baclofen
o Tremor propranolol
definition of Parkinson’s Disease
progressive reduction of dopamine in the basal ganglia (substantia nigra) leading to movement disorder
Causes of Parkinson’s disease
- Unknown genetic Factor, environmental factor
- Most commonly sporadic mutation in genes SNCA, Parkin, PINK-1, DJ-1, TREM2, MHFTR and LRRK2
- Reduction of dopamine in the BG
types of Parkinson’s Disease
• 2 subtype
o Juvenile < 21 yrs
o Young onset – 21-40 yrs
clinical features of Parkinson’s Disease
triad of resting termor, rigidity & bradykinesia
• Unilateral tremor:
4/6 hz, pillrollling tremor
Asymmetrical
Worse at rest
Improves wit intentional movement
• Cogwheel ridgitiy
• Bradykinesia: movement gets slower and smaller
Handwriting gets smaller and smaller
Take only small steps (shuffling gait)
Difficulty initiating movements (standing still to walking)
Difficulty turning around when standing
Reduced facial movement and facial expression (Hypomania)
• Conjugate gaze disorders jerky (saccadic) pursuit and falling short of intended target (hypometric saccades)
• Depression
• Sleep disturbance and insomnia
• Loss of the sense of smell (anosmia)
• Postural instability imbalance or falling
• Cognitive impairment and memory problems dementia
ix for Parkinson’s Disease
- Clinical features are diagnostic
- Dopaminergic agent trial Used in diagnostic uncertainty symptom better
- MRI Brain used when diagnostic uncertainty absence of dorsolateral nigral hyperintensity on 3.0 Tesla susceptibility weighted scan
Mx of Parkinsons’ Disease
• Monoamine oxidase-B (MAO-B) maybe used as 1st line in very mild symptoms
o Rasagiline for monotherapy or combined use
o Selegiline adjunct only
• Dopamine agonist
o pramipexole, ropinirole, transdermal rotigotine
o 1st line in < 70 – less risk with dyskinesia
• Levodopa: Synthetic dopamine combined with drug that stops body breaking down levodopa (carbidopa and bensesarizde)
o 1st line in > 70
o Domperidone for N+V, levodopa can cause N+V
• Anticholinergic agents only treat mild symptoms * use as adjunct
o Trihexyphenidyl, amantadine
• Combination drugs co-benylidopa (levodopa and benserazide) and co-careldopa (levodopa and carbidopa)
• COMT: prolongs duration of levodopa
o Entacapone, tolcapone, opicapone
• Deep brain stimulation treat disabling tremor
what is tension-type headache
• Generalised headache with a predilection for involving the frontal and occipital regions with tight band type headache
what are the differernt types of tension headaceh
- Infrequent episodic less than one day of headache per month.
- Frequent episodic at least 10 episodes of headache occurring on average 1–14 days per month for more than 3 months.
- Chronic 15 or more days of headache per month for 3 or more months.
aetiology of tension headache
- Muscle aches in frontails, temporalis and occipitalis
- Psychological stresses are the most common trigger
- Distrubed sleep pattern can also be a trigger
RF for tension headache
- Stress
- Depression
- Alcohol
- Skipping meals
- Dehydration
- Female
- 20-39 yrs old
clinical features of tension headache
- Classical headache which produces a band like pattern around the frontal and occipital region
- Non-throbbing headache
- Constricting pain
- Last minutes to day
- Not aggravated by daily activities e.g. walking.
- General muscle tenderness in the head
- Rare photophobia or phonophobia, regular analgesic use, anxiety and depression
Ix for tension headache
• Clinical diagnosis
neuro exam to exclude other red flags
Mx of tension headache
- Reassurance
- Episodic: Basic analgesia: paracetamol, NSAID’s, aspirin
- Chronic: 10 sessions of acupuncture over 5-8 weeks
- Relaxation techniques, antidepressants (amitriptyline)
- Hot towels to local area.
what is migraine
• chronic, genetically determined, episodic, neurological disorder that usually presents in early to mid-life
what are the different types of migraine?
• Migraine without aura
Recurrent headache disorder manifesting in attacks lasting 4 – 72 hours
Unilateral location, pulsating quality, moderate or severe intensity
Aggravated by routine physical activity
Nausea, photophobia and phonophobia
• Migraine with aura
Recurrent attacks
Unilateral fully reversible visual lasting minutes precedes headache
• Silent migraine
aura symptoms without the headache
• Hemiplegic migraine
Migraine with aura + motor weakness
aetiology of migraine
- Unknown
* Related to dilatation and constriction of blood vessels.
pathophysiology of migraine
- Neurovascular disorder neuro event precede and initiate headache
- Neurogenic inflammation of first division trigeminal sensory neuros which innervate the large vessel and meninges of the brain
RF for migraine
• CHOCOLATE CHocolate Oral contraceptive Caffeine (Or withdrawaL) Alcohol Travel Exercise
clinical features of migraine with or without aura
- 4-72 hrs
- Moderate to severe intensity
- Worsened by normal activity” walking/bending/climbing stairs.
- Pounding and throbbing in nature
- Usually unilateral but can be bilateral
- photophobia
- phonophobia
aura Sparks in vision Blurring vision Lines across vision Loss of different visual fields. Zig zag Scotoma. Occur 15-60 minutes before attack caused by reduced blood flow to the occipital cortex before an attack. Can also have sensory (pins and needles) and speech aura • Nausea and vomitting.
clinical features of hemiplegic migraine
• Hemiplegic migraine Mimic stroke and you must exclude this fast Typical migraine symptoms Sudden or gradual onset Hemiplegia Ataxia Changes in consciousness.
what are the different stages of migraine
Premonitory/prodromal (3 days before headache)
Aura – lasting upto 60 minutes before headache
Headache -4-72 hrs
Resolution – headache resolves by sleep/vomiting
Postdromal or recovery phase.
mx for migraine
• Acute Medical management
Paracetamol
Triptans sumatriptan
NSAID’S (ibuprofen/ naproxen)
Antiemetics if vomiting occurs (metoclopramide)
Sodium valproate can be used, but not in pregnancy
Caffeine can also be used to relieve pain
• Prophylaxis
Propranolol
Topiramate (not in pregnancy- causes cleft palate)
Amitriptyline
Magnesium sulfate
• Acupuncture – Rx and prophylactic
• Supplementation with vitamin B12 – can reduce frequency and severity.
• Menstruation migraine- prophylactic NSAID’s (mefenamic acid) or triptans (fovatriptan or zolmitriptan)
