Neurology Flashcards
Branches of aortic trunk? R CCA and L CCA bifurcate at what level? Ascend in what structure? Once in cranial cavity run in what?
Brachiocephalic trunk--> R common carotid and right subclavian arteries L common carotid L subclavian Approx C3-C4 Carotid sheath Cavernous sinus
Cervical internal carotid has no what? Anterior and medial to what? Posterior and lateral to what? Ascends behind and then medial to what?
Narrowings/ dilatations/ branches Internal jugular vein ECA at origin ECA (Rare carotid-basilar anastomoses)
Petrous ICA penetrates what bone and runs horizontally in what? Small branch where and small potential connection with what?
Temporal bone- anteromedially in carotid canal
Middle/ inner ear- caroticotympanic artery
ECA- vidian artery
Turns superiorly at what? Enters what thing? Pierces dura at level of what? Small branches supply what 3 things Potential small connections with ECA via what?
Forman lacerum Cavernous sinus Level of anterior clinoid process Dura, cranial nerves 3-6 and posterior pituitary ILT
Ophthalmic artery is usually what and passes into what? Superior hypophyseal arteries/ trunk supply what? Posterior communicating artery runs backwards above what to connect with the PCA? Anterior choroidal artery supplies what things?
Intradural- into the optic canal
Pituitary gland, stalk, hypothalamus and optic chiasm
CN3 to connect with PCA
Choroid plexus, optic tract, cerebral peduncle, internal capsule and medial temporal lobe- for vision and motor control
What the middle cerebral artery? M1 runs laterally to what? M2 runs in what? M3 emerge onto the what? M4 are what?
Larger of the 2 terminal ICA branches Laterally to limen insulae In the insular cistern The brain surface Vessels on the brain surface
What does M1 supply?
Lentiform nucleus (putmen and globus pallidus)
Caudate nucleus
Internal capsule
What is the anterior cerebral artery? A1 runs medially to connect with contralateral ACA via what? A2 runs in interhemispheric fissue to what? A3 are cortical branches from what arteries?
Smaller of 2 terminal ICA branches
Via anterior communicating artery
Genu of corpus callosum and 2 cortical branches
Callosomarginal and pericallosal arteries
Vertebral arteries arise from what? Enters foramina transversarium at what level? Turn laterally at what? Loop posteriorly on what? Through foramen magnum anterolateral to what?
Subclavian arteries- left may directly from arch C6 C2 C1 Medulla
Extracranial VA branches supply what?
Neck muscles, spinal meninges(cervical spine,) spinal cord- cervical cord, anastomoses with other neck vessels- ECA branches
Intracranial VA branches?
Anterior spinal artery, small meduallary perforators, posterior inferior cerebellar artery (PICA) supplies medullar and inferior cerebellum
The VAs unite to form what? Runs anterior to what? Multiple perforating arteries to what? Bilateral anterior inferior cerebellar arteries supply what? Also what arteries?
Basilar artery Pons Brainstem Cerebellum, 7&8 CNs Bilateral superior cerebellar arteries (SCAs)
The 2 PCAs arise from what? Partially encircle what to supply what things? Also, the medial and lateral posterior choroidal arteries supply what things?
Terminal bifurcation of the basilar artery
Midbrain—> thalamus, geniculate bodies, cerebral peduncles and tectum
Tectum, thalamus and choroid of the 3rd and lateral ventricles
What cortical territories does the posterior cerebral artery supply?
Inferior temporal lobe- anastomoses with the MCA vessels
Posterior third of the interhemispheric surface- anastomoses with the ACA
Visual cortex and occipital lobe
Classification of headaches?
Primary- tension, cluster, migraine, secondary- meningitis, encephalitis, GCA, medication overuse, venous thrombosis, tumour, SAH
Other- trigeminal neuralgia
Red flags for headaches?
Fever, photophobia/ neck stiffness, new neurological symptoms, dizziness, visual disturbance, sudden onset occipital headache, worse on coughing/ straining, postural, worse on standing/ lying/ bending over, severe enough to wake the patient, vomiting, history of trauma, pregnancy (pre-eclampsia)
History for headaches?
Time, pain- severity, quality, site and speed, associated, triggers +/-, response- during attack/ function/ medication useful, between attacks- normal persisting symptoms, any change in attacks
Examination for headaches? Fundoscopy to look for what?
Fever, altered consciousness, neck stiffness, Kernigs sign, focal neurological signs- fundoscopy, always check BP also
Papilloedema- indicates raised intracranial pressure- may be due to brain tumour, benign intracranial hypertension or intracranial bleed
Symptoms of a migraine?
Visual/ other aura lasting 15-30 mins followed by unilateral, throbbing headache/ isolate aura with no headache
Episodic severe headaches without aura- often premenstrual, usually unilateral, with nausea, vomiting +/- photophobia/ phonophobia, may be allodynia
Criteria of migraine with no aura?
> 5 headaches lasting 4-72h + nausea/ vomiting (or photo/ phonophobia) + any2 of: unilateral, pulsating, impairs/ worsened by routine activity
1 of: nausea and/or vomiting, photophobia and phonophobia
2 criteria of migraine with aura?
> 1 reversible aura symptom: visual- zigzags, spots, unilateral sensory- tingling, numbness, speech- aphasia, motor weakness- ‘hemiplegic migraine’
2 of: >1 aura symptom spreads gradually over >5m and/ or >2 aura symptoms occurring in succession, each aura symptom lasts 5-60m, >1 aura symptoms is unilateral, aura accompanied/ followed within 60m with headache
Triggers for migraines (CHOCOLATE)?
Chocolate, hangovers, orgasms, cheese, oral contraceptive pill, lie-ins, alcohol, tumult, exercise
DD for migraine? Tx?
Cluster/ tension headache, cervical spondylosis, increased BP, intracranial pathology, sinusitis/ otitis media, caries, TIAs may mimic migraine aura
NSAIDs- ketoprofen and dispersible aspirin= similar efficacy to oral 5HT agonists- triptan and ergot alkaloids
Non-pharm= warm/ cold packs to the head, rebreathing into paper bag may help abort attacks
Avoid triggers, stop pill
X3 prophylaxis= propanolol/ topiramate, acupuncture, amitriptyline
Features of cluster headache? Presentation?
May be due to superficial temporal artery smooth muscle hyperreactivity to 5HT- there are hypothalamic grey matter abnormalities too, autosomal dominant gene= role too, onset at any age; commoner in smokers
Rapid onset severe unilateral, orbital, supraorbital/ temporal pain
15-180 mins long, middle of night/ morning hours after REM sleep usually
Other symps: ipsilateral eye lacrimation and redness, rhinorrea, miosis and/ or ptosis
Tx of cluster headaches?
Acute= subcut sumatriptan, 100% O2 through non-rebreathable mask for 15 mins Prevention= veramipil, lithium carbonate, prednisolone
Classification and cause of tension headaches?
Episodic TH- <15d per month, chronic TH- >15d per month, can med induced, also ass with depression
Neurovascular irritation refers to scalp muscles and soft tissues
Presentation and tx of tension headaches?
Generalised mild-mod pain pressing/ tightening pain bilaterally
30 mins- 7 days
Simple- ibuprofen, aspirin
Chronic- TCA e.g. amitriptyline
4 criteria of trigeminal neuralgia?
> 3 attacks of unilateral facial pain, pain in >1 division of trigeminal nerve with no radiation, pain must 3 of: paroxysmal attacks lasting from 1-180 seconds, severe intensity, electric shock-like/ shooting/ stabbing/ sharp, precipitated by innocuous stimuli to affected side of face, no neurological deficit
Tx of trigeminal neuralgia?
1st line= carbamezapine 100mg
2nd and 3rd line= lamotrigine, phenytoin or gabapentin, surgery= rhizotomy, stereotactic radiosurgery etc
Presentation of GCA headache?
Tender, thickeneded, pulseless temporal arteries, jaw claudication- pain on chewing, scalp tenderness–> pain on combing hair, visual disturbance–> amaurosis fugax (can be irreversible,) systemic features–> malaise, fever, lethargy, weight loss, polymyalgia rheumatic features
Invest and tx of GCA?
Bloods= -ANCA, ESR>50, raised CRP and ALP, lowered Hb
Temporal artery biopsy- necrotising arteritis with inflammation
High dose prednisolone (40mg)+ low dose aspirin (75mg)
PPI and bisphosphonate also
Symptoms of CNS infection? Non-blanching rash? 20% bac meningitis sufferers have what?
Headache, neck stiffness, photophobia, altered consciousness
Meningococcal septicaemia
Skin scars, amputation, hearing loss, seizures, brain damage
Bacterial causes of meningitis- acute and chronic? Fungal chronic? Acute viral?
N.meningitidis, s.pneumoniae, listeria spp, group B strep, h. influenzae B, e.coli
Mycobacterium (TB,) syphilis
Crytococcal
Herpes simplex, varicella zoster, enterovirus
Advice to GP for meningitis tx? >1hr what ABs alternatively? In hospital? For N.mengitidis?
IM benzylpenicillin 1200mg if signs of meningococcal disease
Cefotaxime, ceftriaxone
ABC, assess GCS, blood cultures within an hour, broad spec ABs, steroids- IV dexamethasone
Identify close contacts, Ciprofloxacin
What is encephalitis? Causes? Non-infective? Clinical pres?
Inflammation of brain parenchyma
Herpes, entero, poliovirus, coxsackie, measles, mumps, varicella
Other: Japanse, tickborne, rabies, West Nile, dengue
AI and paraneoplastic
Flu-like, fever, headaches, confusion, nausea, vomiting, altered GCS, cognitive impairment, seizures, +/- meningism
Invest and tx for encephalitis?
MRI head within 24-48 hours, lumbar puncture- lymphocytic CSF, viral PCR
Mostly supportive, IV acicyclovir is suspected HSV/ VZV within 30 mins, phenytoin for seizures
Initial infection with herpes zoster is what? Reactivation? Varicella lies dormant in what? RFs for reactivation? Present? Give what?
Chickenpox
Shingles
DRG
Old age, poor immune system, chickenpox <18 months age
Dermatomal distribution of rash and pain
Oral acyclovir
Ascending sensory system has what things? Lat spinothalamic tract crosses where? Descending motor system?
Posterior columns, lat spinothalamic tract, thalamus
Internal capsule, pyramidal decussation, corticospinal tract
Reticular activating system is peri-aqueductal gray matter/ floor of fourth ventricle leading to what?
Alertness, sleep/wake, REM/ non REM sleep, respiratory centre, cardiovascular drive
MRI images- colour of T2 and T1? Disorders affecting brainstem?
White and black
Tumour- meningioma, schwannoma, astrocytoma, metastasis, hemangioblastoma, epidermoid
Inflammatory- MS, metabolic- central pontine myelonecrosis, trauma, sponta haemorrhage- AVM, aneurysm, infarction- vertebral artery dissection, infection- cerebellar abscess from ear
Criteria for brainstem death? Location for common benign tumours?
Pupils, corneal reflex, caloric vestibular reflex, cough reflex, gag reflex, respirations, response to pain
Cerebellopontine angle
What is MS? Typically presents in who? Common sites? Types?
Chronic AI disorder of CNS- plaques of demyelination
Optic nerves, brainstem, cervical spinal cord
Relapse and remitting, primary progressive, secondary progressive
Typical MS symptoms?
Optic neuritis, spasticity and other pyramidal signs, sensory S&S, Lhermitte’s sign, nystagmus, double vision, vertigo, bladder and sexual dysfunction
Ix of MS? Management?
MRI brain and spine, evoked potentials, LP= oligoclonal IgG bands in CSF
Acute: steroids= methylprednisolone, chronic: 1st line= beta interferon, glatiramer acetate, 2nd line= natalizumab
Symptoms- tremor= BB, spasticity= baclofen, PT, OT, MDT
What is epilepsy? Prodrome then what x3?
Recurrent tendency to have spontaneous, intermittent and abnormal electrical activity in a part of the brain, manifesting as seizures.
Prodrome–> aura–> ictal symptoms- dependent on part of brain affected–> post-ictal symptoms- headache, confusion, amnesia etc
What are partial (focal) seizures? Symptoms of temporal, frontal, occipital and parietal?
Limited to one hemisphere
Temporal= smell/taste abnormalities, auditory phenomena, automatisms- lip smacking, walking without purpose, memory phenomena- deja-vu
Frontal: motor phenomena, may –> to Jacksonian march(spreading clonic movement)
Occipital–> visual phenomena
Parietal–> sensory disturbances- tingling, numbness etc.
What are generalised seizures? Absence? Myoclonic? Tonic? Tonic-clonic? Atonic?
Simultaneous LoC<10s, abrupt onset and termination
Myclonic= sudden, brief jerking of limb/ face/ trunk
Tonic= increased tone
Tonic-clonic: 1) Tonic phase- LoC and increased tone of limbs 2) Clonic phase (rhythmical jerking of limbs)
Atonic= no LoC, sudden loss of muscle tone e.g. drop of hand or fall
Seizure treated with carbamazepine, lamotrigine? Sodium valproate? Valproate? Valproate, ethosuximide? Valproate/ levetiracetam? Carbamazepine is CI in what seizures?
Partial(focal) Tonic-clonic Tonic, atonic Absence Myoclonic
Tonic, atonic, absence and myoclonic
What is status epilepticus? Tx in community, hospital? If seizures continue?
Seizure>5m- emergency
Open and maintain airway, give O2 and gain IV access
Community–> buccal midazolam or rectal diazepam
Hospital–> IV lorazepam/ diazepam
Phenytoin
What is SUDEP? More common in what?
Sudden unexpected death in epilepsy- in uncontrolled epilepsy and may be related–> nocturnal seizure-ass apnoea or asystole
What is non-epileptic attack disorder?
Uncontrollable symptoms, no learning disabilities, and CNS exam, CT, MRI, and EEG= normal, may coexist with true epilepsy
Changes in behaviour, sensation and cognitive function caused by mental processes ass with psychosocial distress
Situational, last 1-20 mins
Dramatic motor phenomenoa or postical atonia
Eyes closed and crying/ speaking
Rapid/ slow postictal recovery
History of psych illness/ other form
Vagal nerve stimulation
What is syncope?
Paroxysmal event- changes in behaviour, sensation and cognitive processes are caused by insufficient blood sugar/ O2 supply to brain
Often situational
Parasyncopeal symptoms- light headed
5-30 seconds, recovery within 30 seconds
Cardiogenic- less warning, history of heart disease
Common for BP and HR to drop
Fainting can involved jerking
Missile and non-missile head injuries? Lesion distribution? Time course damage following injury? Focal and diffuse damage after non-missile trauma?
Dura mater remains intact
Diffuse, focal
Primary- immediate biophysical forces of trauma, secondary- sometime after, physiological responses, effects of hypoxia, infection
Focal= scalp, contusions, lacerations, skull= fracture, meninges= haemorrhage, infection, brain= contusions, lacerations, haemorrhage, infection
Diffuse axonal injury, vascular injury, hypoxia- ischaemia, swelling
Blunt head trauma? Focal damage? Angled/ pointed objects–> what fractures? Flat surfaces?
Focal damage- scalp lacerations
Skull fracture, implies considerable force, increased risk of haematoma, infection and aerocele
Localised - often open/ depressed
Linear fractures- can extend–> skull base (contrecoup fractures)
People affected by subdural haematomas? Why? Cause of bleeding? Levels of consciousness?
Elderly and alcoholics
Brain atrophy, vein stretching, increased likelihood to fall
Rupture of bridging veins running from cortex–> venous sinuses
Fluctuating levels, ICP gradually rises over some weeks
Cause of bleeding from extradural haematoma? Level of consciousness? x4 features of ICP?
Fracture of temporal bone–> tear of middle meningeal artery
Brief period- then lucid interval of improvement, then condition rapidly deteriorates as ICP increases
Headache, vomiting, confusion, seizures
Investigation of subdural and extradural haematomas? Why is LP contraindicated? What shaped is extradural? Subdural?
CT head
Coning
Egg-shaped
Sickle-shaped
Management of SDH and EDH?
ABCDE= first, then osmotic diuresis with mannitol to treat raised ICP, surgery: SDH- emergency evacuation via Burr hole craniotomy, EDH= clot evacuation
Aetiology of subarachnoid haemorrhage? RFs?
Usually result of bleeding from berry aneurysm at branching points of Circle of Willis- origin of anterior comm artery, joining of pos comm artery with ICA
Congenital AV malformations
Idiopathic
Smoking, alcohol, HTN, bleeding disorders, Marfan + ED syndromes, autosomal dominant PKD
Pres of SAH?
Sentinel headache in 3 weeks prior to SAH due to small warning bleeds
Symps= sudden onset severe occipital thunderclap headache, others= nausea, vomiting, neck stiffness, seizures, drowsiness
Signs= meningism, fundoscopy- intraocular haemorrhages, signs of increased ICP, focal neurology e.g. pupil changes and other signs of 3rd nerve palsy if pos comm artery aneurysm
Invest and tx of SAH?
CT head= white star-shape due to blood in basal cisterns
Lumbar puncture- wait 12 hours= xanthochromia(yellowing)= breakdown of RBCs–> increased bilirubin
Nimodipine- decreases cerebral artery vasospasm so prevents cerebral ischaemia
Surgery- coiling(endovascular obliteration) preferred to clipping
2 key surface antigens on influenza A? Types in humans?
Haemagglutinin(15 subtypes)- virus binding and entry–> cells i.e. grappling hook for getting in
Neuraminidase(9 subtypes)- Bolt Cutters for getting out
H1-H4, N1-N2 and maybe H5
Genetics of influenza? Why are there seasonal epidemics?
8x single-stranded RNA segments, gene re-assortment can happen in infections as genome= segmented
Genes swapping during co-infection with human and avian flu virus
No proof reading mechanism= prone to mutation
Antigenic drift
Influenza B features? C? Transmission? Infection and comps?
Prone to mutation, sporadic outbreaks less severe, often children
Minor disease, mildly symptomatic/ asymptomatic
Aerosols, coughs and sneezes, hand to hand, other contact
Upper and/or lower symptoms+ fever, headache, myalgia, weakness
Bacterial pneumonia, mortality higher with underlying health conditions- chronic cardiac and pulm diseases, old age, chronic metabolic disease, chronic renal disease, immunosuppressed
Tx options for influenza? Peaks when? Incubation? Infections from symptoms= days after?
Supportive- oxygenation, hydration/ nutrition, homeostasis maintain, prevent/ treat secondary infections
Antivirals to reduce transmission, severity and duration
1-4 days, 4-5 days after
December-March
Avian flu features? Most seasonal flu=? Controlling?
Ruffled feathers and depression, mutation–> highly pathogenic= 100% mortality
SE Asia- close proximity poultry and people, 50-80%= in small rural households
Secondary bacterial pneumonia, H5N1= primary viral pneumonia
Cull affected birds, quarantine, biosecurity, vaccination, antivirals, PPE, reduced risk co-infection
Swine flu features? Managing early stages flu?
Reassortment swine, avian and human flu, different from human flu
Sensitive to Oseltamivir and Zanamivir, seasonal not effective
40+ some immunity
Containment phase- case identify- swabs, case Tx, contact tracing, increased prophylaxis, tx phase= treat cases only, National Flu Pandemic Service
Infection control measures? Managing cases?
Hand hygiene, cough etiquette, universal precautions and PPE, surgical masks, non aerosol generating procedures, patient segregation, reduced social contact, flu surgeries
Call centres, non-medical= algorithm, patient/ relative= antivirals, home delivery, hospital admission criteria
Anti-viral drugs how many courses to cover what % attack rate? Most effective when? Issues?
30 million for 50% attack rate
Mostly Tamiflu and some Relenza, within 24-48 hours
Reduced hosp admission by 50% and disease duration by 24 hours
Resitance, side effects, who given, distribution
Limited role of face masks?
Only if worn correctly, changed freq, removed properly, disposed safely, used + good universal hygiene procedure, run out, how many per day?
Staff issues with flu? Impact on schools and other services? Pop-wide interventions?
Anxiety to work, adequate protection, access to antivirals, risk to family, staff segregation, redeployment, staff recycling, organisations sharing staff
NHS staffing if schools close?, distribution and transport, prisons, education, business
Travel and mass gatherings, restrictions, school closures, voluntary home isolation, screening people into UK ports
MERD coronavirus? SARS?
Bats–>camels, lots of outbreaks due to Hajj
Caused by SARS-COV virus
What are adverse events a product of? What are sharp-enders more likely to be? What model of causation? What is culture?
Many causal factors
The inheritors rather than the instigators, remedial efforts directed at removing error traps and strengthening defences
‘Swiss-cheese’ model
Shared values and beliefs that interact with an organisation’s structure and control systems–> behavioural norms
What is healthcare harm? Occupational and transport safety figures focus on what more? What is human error?
Broadly defined- includes smaller/ less serious events and larger events and fatalities
On mortality and larger incidents of harm
Failure of a planned action/ sequence of mental/ physical actions to be completed as intended/ use of wrong plan achieve an outcome
What are never events? Latent failure? Active failure? Organisational system failure? Technical failure?
Serious, largely preventable patient safety incidents if correct measures implemented e.g. wrong site/ implant, retained object, wrong rate of admin etc
Removes practitioner- organisational policies, procedures, resource allocation= less apparent
Direct contact with the patient
Indirect involving management, culture, knowledge
Indirect failure of facilities/ external factors
3 factors contributing to adverse events? Confirmation bias? Anchoring? Diagnosis momentum? Flow?
Clinical complexity, poor communication- good= SBAR, complex systems
Evidence to confirm rather than discomfirming evidence e.g. tests
Lock onto salient features in initial presentation and failing to adjust in light of later information
Once labels are attached, gathers momentum until becomes definite and all other possibilities excluded
Error–> report–> learn from it–> share it–> inform patient and apologise (duty of candour)
Distinguishing motor neurone disease from MS and polyneuropathies? From myasthenia gravis?
No sensory loss/ sphincter disturbance
Eye movements not affected
Features of UMN disease?
Hyper-reflexia, hyper-tonia, spasticity, Babinski +ve, DISUSE ATROPHY
Hypo-reflexia, hypo-tonia, denervation atrophy, Babinski -ve
Features of MN disease?
Dysfunction of MOTOR neurones, no sensory disturbances, destruction in anterior horn cells of brain and spinal cord
4 types= most patients= mixed picture, ALS= most common, SOD-1 gene
Meaning of paresis? Paralysis? Ataxia? Apraxia?
Impaired ability to move body part
Can move body part- no will
Will movements= clumsy, ill-directioned/ uncontrolled
Disorder of consciously organised patterns of movement/ impaired ability to recall acquired motor skills
What can affect UMN and LMN? Investigating UMN disease? Median age and how many years fatal?
Fasciculations- varied picture
EMG, raised creatinine kinase due to muscle destruction
60 years, 2-4 years
Tx for MN disease?
Anti-glutamatergic drugs: Riluzole- Na+ channel blocker inhibiting glutamate, CI= renal/ liver, prolongs life 3 months, SE= vomiting, pulse increase, somnolence, headache, vertigo, LFT increases
Symptoms= tracheostomy, ventilator, NG tube
PT/OT/ MDT
Drooling= amitryptyline, propantheline
Joint pain and distress= NSAIDs, then opioids
Death= due to resp failure due to pneumonia
3 cardinal symptoms of brain tumour? Features of increased ICP? Cardinal physical sign?
Raised ICP–> headache, reduced conscious level, nausea, vomiting
Progressive neurological deficity, epilepsy- more focal seizures
Worse in morning, increased by coughing, sometimes relieved by vomiting
Papilloedema
Causes of secondary tumours? Tx options?
Non small cell lung tumour, small cell lung, breast, melanoma, renal cell, GI, unknown primary
Chemo/radiotherapy, surgery, best supportive care
Surgery for: absent/ controlled primary disease, age<75, good performance status
Most primary where origin? Most freq, that occur in adults? Most common in 4th-5th decade?
Glial cell
Astrocytoma
Oligodendroglioma
Gliomas graded what? Grade I? II? III? IV?
Pilocytic-‘Paediatric’
Benign- premalignant
Anaplastic astrocytoma- cancer (malignant)
Glioblastoma multiforme(GBM)- most common phenotype, given time= all gliomas–> GBM, prognosis=<1 year
2 pathways–> malignant gliomas?
1) Common= initial genetic error of glucose glycolysis, mutation of IDH-1–> excess of 2-hydroxyglutarate, gen instability in glial cells and inappropriate mitosis
2) Less common= no IDH mutation, catastrophic gen mutation, poor prognosis- even low grade
How classify brain tumours? Aim to determine what?
Histologically A and E, immunohistochemistry and mol/ cytogenetics
Tumour type, grade, prognostic factors, additional markers
Tx of brain tumours?
Temozolomide- smaller pro-drug crosses BBB, methyl–> guanine preventing DNA replication- can be reversed by MGMT from tumours–> resistant
Chemo and radiotherapy
Dexamethasone- most powerful oral/IV, improves brain performance in all tumours, reduced inflam and oedema, no later than 2pm
Most common cancers metastasising to brain?
Lung, breast, colorectal, prostate
Commonest cause of dementia? Early degeneration of what brain section? Frontal lobes? Temporal lobes?
Alzheimers disease- medial temporal lobe–> temporal neocortex, frontal and parietal ass areas
Motor movements, motor speech-Brocas area, personality, planning
Hearing, language comprehension, semantic knowledge, memory, emotional behaviour
Selective amnesia and language impairments–>complex attention–> visuospatial, sustained attention–> global deficits
Differentials of dementia?
Vascular/ mixed dementia- sub-cortical frontal pattern- attention and motor difficulties, visuospatial difficulties
With Lewy bodies- fluctuating cognition, pronounced disturbances in attention, working memory and early visuoperceptual deficitis
Depressive pseudodementia
Psych changes in dementia?
Subtle behavioural changes- inattentiveness, mild cog dulling, social and emotional withdrawal and agitation
Apathy, disengagement
Psychotic= delusions, hallucinations, anxiety
Pre-clinical AD?
Memory impairment= first marker, poor perf on episodic memory tests, general cog function= preserved, daily living= intact, score above 24/30 on MMSE, high risk–> AD
Examination for AD?
History- cog function via 6 CIT- year, month, address, with 5 parts, count 20-1, months in year in reverse, repeat address
Blood tests- B12, folate, iron, neuropsychology
MRI- atrophy, function assessed- energy and blood supply= PET and SPECT, functional MRI- networks
Management of dementia?
Prevention= healthy behaviours, support= socially and cognitively, carers courses
Meds for mood and anxiety- acetylcholinesterase inhibitors- memantine (anti-glutamate,) control vasc factors
What are somatisation disorders? Conversion disorder? Pain disorder? Dissociative disorders?
When physical symptoms caused by mental/ emotional factors
No medical explanation for brain/ neurological symptoms
Persistent pain cannot be attributed to physical disorder
Cause physical and psychological problems, short lived/ longer
Of movement/ sensation
Dissociative dementia- info about themselves, past, skill, not knowing how got there
Dissociative identity disorder- uncertain about identity, may feel presence of others
Who’s hierarchy of needs? ABC of self-care?
Maslow’s
Awareness
Balance
Connection
What is myasthenia gravis characterised by? Associated with what in 10%
Weakness and fatigability of ocular, bulbar and proximal limb muscles- ptosis, talking and chewing problems, swallowing
IgG ABs–> AChR at post-synaptic membrane at NMJ
Thymic tumour
What drugs can aggravate myasthenia gravis? Investigations?
BBs, lithium, some ABs
Bedside- count to 50/ keep arm outstretched
Bloods- anti-AChR ABs in blood, anti-MuSK ABs
Tensilon test(rarely performed)
CT/MRI for thymoma
Tx for myasthenia gravis?
Anticholinesterases- pyridostigmine, immunosupressants- prednisolone, azathioprine
Plasmapheresis- IVIG in myasthenic crisis
Thymectomy
What is expert medical generalism?
HC–> all patients on list with any HC need
Focus on whole person
Only output of cerebellum? Symptoms of cerebellar ataxia? Examination?
Purkinje cells
Slurring speech- staccato, swallowing difficulties, oscillopsia, clumsiness, tremor, loss precision, unsteadiness in dark, stumbles and falls
Gait, limb ataxia, eye movements, speehc, sensory ataxia, other signs
Signs of cerebellar dysfunction? (DASHING)
Nystagmus, dysarthria, action tremor, dysdiaochokinaesia- impaired ability rapid movements, truncal ataxia, limb and gait ataxia
Clinical severity ataxia?
Mild= mobilising independently/ walking aid, moderate= 2 walking aids/ frame, severe= wheelchair dependent, SARA= rating and assessment of ataxia
Majority of children brain tumours where? Adults? Most meningiomas what grade?
Posterior fossa
Supraentorial
Grade I
Normal ICP in adults? Types of herniation syndromes?
<15mmHg
Uncal herniation
Tonsil herniation
Subfalcian (cingulate) herniation
Formation of dopamine? Where is it produced? 3 cardinal triad of Parkinson’s?
L-tyrosine–>L-DOPA–>dopamine
Substantia nigra- apoptosis here–> PD
Tremor- worse at rest, 4-6 cycles/ sec= slower than cerebellar tremor
Rigidity/tone–> ‘cogwheel rigidity’, felt during rapid pronation/ supination
Brady/ hypokinesia- slow to initiate movement, low amplitude excursions in repetitive actions, reduced arm swing, festinance- shuffling, freezing at obstacles, expressionless face
Causes of Parkinson’s?
Reduction in dopamine secreting cells of substantia nigra- lightens, reduce dopamine to striatum, reduced neuronal transmission from basal ganglia to cortex
Diagnosing Parkinson’s?
Tremor and/or hypertonia with bradykinesia; exclude frontotemporal dementia and cerebellar disease
Signs worse on one side
MRI rule out structural pathology
Differentials for Parkinson’s?
Benign essential tremor
Parkinson-plus syndromes- VIVD- vertical gaze palsy, impotence/ incontinence, visual hallucinations, interfering activity by limb, diabetic/ htn patient
Drugs- antipsychotics, metoclopramide, prochlorperazine
Rarer= trauma, Wilson’s disease, HIV
Drugs to increase dopamine supply? Decrease dopamine breakdown? Help tremor?
Co-careldopa- L-DOPA (levodopa)+ carbidopa
Dopamine receptor agonists–> ropinirole/ rotigotine
MAO-B inhibitor–> rasagilline/ selegiline
COMT inhibitor–> entacapone/ tolcapone
Anticholinergic- amantadine
Non-pharm for Parkinson’s?
Deep brain stimulation, surgical ablation of overactive basal ganglia
Cardinal features of Huntingdon’s disease?
Chorea- fidgety (not aware of abnormal movements), dementia, psychiatric issues-pers change, depression, psychosis+ FH
What triplet of Huntington gene is repeated? Atrophy of which part of the brain–> depletion of GABA? Early features?
CAG>39 repeats needed
Striatum
Depression, self-neglect, irritability, behavioural issues etc.
Advanced= chorea and rigidity, dementia
Differentials for HD?
Sydenham’s chorea, benign hereditary chorea, drug induced, other dyskinesias, other causes of dementia
HD examination?
Abnormal eye movements, chorea, ataxia- heel–>toe walking issues, ‘touch of Parkinsonism’- rigidity, slowness fine finger movements
Conventional HD tx?
Chorea- neuroleptic- sulpiride, depression= SSRIs- seroxate, psychosis= neuroleptic- Haloperidol, aggression= Risperidone
What is Guillain Barre-syndrome? Triggered by what infections?
Acute neuropathy, inflammatory and demyelinating
Campylobacter jejuni, EBV, CMV
Presentation of Guillain Barre?
Progressive onset limb weakness after viral illness, loss of reflexes, often sensory and motor disturbances
Severe–> resp depression, vital capacity should be monitored if suspected
Investigations of Guillain Barre? Tx?
Mainly clinical, nerve conduction studies, LP= high protein in CSF
IVIG, ventilation if resp muscles involved
What is the cauda equina? Causes of compression? Presents? Diagnosis and tx?
Bundle of spinal nerves from level L1/2
Back pain, saddle anaesthesia, loss of bowel/bladder control
MRI
Surgical decompression
Nerves affected by mononeuropathies? Causes of polyneuropathies? (DAVID)
Median, radial, sciatic, common peroneal
Diabetes, alcohol, vit def- B12, infective- GB, drugs (isoniazid)
Causes of carpal tunnel syndrome? Tests? Tx?
Pregnancy, obesity, hypothyroidism, RA
Tinnel’s and Phalen’s
Pain relief, splint, steroid injection, surgery
Aetiology of TIA and stroke?
Thrombosis in situ, embolism from heart(valve disease, mural thrombus- AF)/ carotid, CNS bleed- ass with HTN, aneurysm rupture, head injury, young patient= vasculitis, thrombophilia, SAH
Modifiable and non-modifiable RFs for stroke?
HTN, smoking, hyperlipidaemia, obesity
DM, male, vasculitis, hypotension
3 features of total anterior circulation syndrome (TACS)- large cortical stroke in ACA/MCA territories?
PACS- partial in ACA/MCA territories?
Contralateral weakness and/or sensory deficit of face, arm and leg, homonymous hemianopia, higher dysfunction- dysphasia, visuospatial disorder
Contralateral weakness, homonymous hemianopia, higher dysfunction
Posterior circulation syndrome (POCS) one of what features? What is Lacunar syndrome? One of what features?
Cerebellar/ brainstem syndrome- quadriplegia, locked in syndrome LoC, isolated homonymous hemianopia, cranial nerve palsy AND contralateral/ sensory deficit
Subcortical stroke due to small vessel disease: pure motor stroke, ataxic hemiparesis- ipsilateral weakness+clumsiness(mostly legs,) pure sensory- contralateral numbness, tingling, pain or burning
Mixed sensorimotor stroke
Clumsy hand dysarthria
Investigation for stroke? 1st and 2nd line for ischaemic? Tx for haemorrhagic?
Distinguish between hemorrhagic and ischaemic stroke –> CT brain
Thrombolysis, then aspirin 300mg for 2 weeks, then clopidogrel 75mg OD
Control BP: B-blocker, Beriplex if warfarin-related bleed, clot evacuation
Rehab= physio, OT, SALT
Anti-hypertensives, statins
What is a TIA?
Sudden onset global neurological deficit lasting <24h, with complete clinical recovery -usually 5-15m
Features of carotid/ anterior blockage? Vertebrobasilar/ posterior?
Hemiparesis- unilateral weakness and/or hemisensory loss
Amaurosis fugax–> descending loss of vision in one eye(ipsilateral retinal/ ophthalmic artery embolism,) Broca’s dysphasia
Hemisensory symptoms
Diplopia, vertigo, vomiting, dysarthria–> slurred speech, ataxia
Hemianopia(ophthalmic cortex) or bilateral visual loss
ABCD2 score for TIA?
Age>/=60= 1 point
BP>/= 140/90= 1 point
Clinical features: unilateral weakness= 2 points, speech disturbance without weakness= 1 point
Duration of symptoms: >60 mins= 2 points, 10-59 mins= 1 point
Diabetes= 1 point
What tx following TIA, if ABCD2>4, >1 TIA/ week/ AF/ on anticoagulant?
Antiplatelet- aspirin 300mg or clopidogrel 300mg unless on anticoagulant therapy
Statin- simvastatin 40mg
If on AC therapy= admit for imaging to rule out haemorrhagic stroke
Secondary prevention following TIA?
Lifestyle, control RFs, clopidogrel and statin prescribed
For patients with 50-90% carotid stenosis= carotid endarterectomy
