Neurology Stroke > Stroke > a syndrome of the sudden onset of focal neurological loss of presumed vascular origin lasting >24h > Transient ischemic attack (TIA) -> a syndrome of the sudden onset of focal neurological loss of presumed vascular origin lasting <24h Posterior circulation stroke Presentation [DR DAN] © Dizziness/vertigo, Right hemianopia, Dysdiadochokinesia, Ataxia, Nystagmus ‘© Usually sudden onset with possible further progression that takes place over hours + May have underlying IHD, hypertension, carotid brults, AF + strokes nthe veRmis > ttuncalataxta Cerebellar lesion ‘* Strokes in the cerebellar lobes ~ limb ataxia ofthe ipsilateral side Presentation [DAN SHIP] + Dysdiadochokinesia, Ataxia, Nystagmus, Slurred speech, Hypotonia, Intention tremor, Past pointing, ‘+ Usually sudden onset with possible further progression that takes place over hours * May have underlying IHD, carotid bruits, AF Cerebellopontine angle stroke -CNS7.8 Brainstem stroke Cetebeltum Presentation [ADD FOG] © AAtaxia © D-Diplopia © D-Dysarthria nystagmus > Cerebellar lesion © F-Facial numbness © 0-Ophthalmoplegia © G-Gaze palsy Diagnosis of acute stroke © Non-contrast CT brain > initial investigation + MRI brain > more sensitivity Cortical vs Brainstem stroke 1. Cortical 2. Brainstem = Focal involvement = Global involvement (whole side) > rule of 4s, see P. 3 F__PLABverse | win plabrersecom 1Neurology Management of acute stroke ‘© Ischemic stroke > Thrombolysis (Alteplase) then, Aspirin 300mg = Cannot be started until a CT-scan has excluded hemorrhage, as they may worsen the bleeding - Thrombolysis is given only within 4.5h of onset of stroke, after 4.5h, it has no significence ‘* Maintain oxygen saturation, glucose control, blood pressure control © Maintain nutrition and hydration + Early mobilization ‘+f time frame isn’t certain or 24.5h has passed following a stroke or CT shows cerebral infarction (which takes time to Cevelop) > Aspirin 300mg Post management stroke ‘© Aspirin 300mg = Clopidogrel 75mg = Aspirin is given for 2 weeks immediately after an ischemic stroke is confirmed by brain imaging = Clopidogrel is given daily long-term = If clopidogrel is contraindicated/not-tolerated > Dipyridamole + low dose aspirin (75mg) ‘© Statin should be offered for all patients following TIAs unless contraindicated Secondary prevention after a stroke or TIA © Lower blood pressure - Aim for 130/80 = DONOTstart controlling BP in the first 48h as this may Eause extension of stroke Lower cholesterol - Aim for 40% reduction in non-HDL cholesterol = Statins can be taken lifelong after TIA orischemic stroke > 80mg Atorvastatin ‘+ Antiplatelet and anticoagulation treatment = _ Notrecommended unless there’re clearindications - If AFis present -> Warfarin, Apixaban (Warfarin Target INR ranges 2.0-3.0) - AF is absent > Clopidogrel 75me daily lifelong, if intolerant > dipyridamole + low dose aspirin - Anticoagulants shouldn’t be started until CT has excluded hemorrhage = Anticoagulants are usually given after 14 days have passed from the onset of an ischemic stroke © Lifestyle adh - Lowsalt diet - Low cholesterol diet = Weight loss + Alcohol reduction + Smoking cessation ‘* Always consider “Carotid endarterectomy” as 2 prevention in TIA + Carotid duplex is used if internal carotid artery is stenosed (stenosis >50% in men, >70% in women) = Should be done within 2 weeks of admission > All people with suspected non-disabling stroke or TIA are considered as candidates for Carotid endarterectomy > Carotid doppler scanning is required first to check for carotid artery stenosis to assess the need for Carotid endarterectomy F__PLABverse | win plabrersecomRule of 4s © 4CNsin: + Medulla = Pons = Above pons + 4Ctis divide evenly into 12 - 3,4,6,12 - Motor nuclei are midline Other CNs don’t divide into 12 © 5,7,8,9,10,11 © Allare lateral ‘4 midline columns + Motor pathway (Corticospinal tract) - Motor nucleus and nerve = Medial longitudinal fasciculus (MLF) = Me © lateral (side) columns = Sympath = Spinothalamic = Sensory nucleus of CNS + Spinocerebellar pathway lemniscus Localizing lesions © Medial_vs. Lateral - Which tractis affected? * Medulla vs. Pons vs. Midbrain - Which cranial nerves are affected? Nerve pathway/chain Neurology MIDBRAIN PONS MEDULLA\ (Ns, Midbrain Pons Tracts Medulla Media --------- Lateral Lesion Olfactory CNA Not in the midbrain Optic CN2 Oculomotor CN3 Not in the midbrain Eye tured out and down (action of LR6 + $04) + ptosis + mydriasis ‘Trochlear CN4 Eye unable to look down when looking towards nose (affected SO) Trigeminal CNS Ipsilateral facial sensory loss, afferent of corneal reflex ‘Abducent CNG Ipsilateral eye abduction weakness (affected LR) Facial CN7 Ipsilateral facial weakness/droop, efferent of corneal reflex Auditory (vestibulocochlear) CNB Ipsilateral deafness or loss of balance Glossopharyngeal CNS ‘Vagus CN10 Ipsilateral pharyngeal sensory loss + impaired swallowing + loss of gag Ipsilateral palatal weakness (absent gag reflex) + vocal cord paralysis ‘Spinal Accessory CN11 Hypoglossal CN12 Ipsilateral shoulder weakness + affected head movement Ipsilateral weakness of the tongue (towards the same side of the lesion) F__PLABverse | win plabrersecomNeurology Midline structures (M) (eterna Can) Contralateral weakness Dinca aca) * Ipsilateral CN motor loss (3,4.6,12) ro ‘+ Ipsilateral intranuclear ophthalmoplegia (INO) Teeny © Contralateral loss of proprioception/vibration Side /Lateral structures (S) Beare el ‘© Ipsilateral Horner’s syndrome ero + Contralateral sensory loss ofp temp Penis Ipsilateral loss of pain/temp in the face Pens aon Ipsilateral ataxia Brainstem blood supply Lateral Medial s Midbrain Pons Medulla tO % The Cranial Nerves “FP __ PLABverse | [Link]Neurology Vascular supply of the brain © ACA~ frontal and medial cerebrum ‘* MCA- lateral part of the hemisphere © PCA- occipital lobe ‘© Basilar artery — cerebellum, brainstem, occipital lobe Medial view Lateralview Middle cerebral artery occlusion = Aphasia in the dominant hemisphere = Neglect in the Non-dominant hemisphere (NN) = Contralateral paralysis (face & arm) © roster conan ter) - Contralateral sensory loss (face & arm) © sicher Mery - Gaze preference toward side of lesion SG Pejc: Pe tery = Homonymous hemianopsia All ore contralateral except the gaze preference Anterior cerebral artery occlusion - Contralateral hemiparesis and sensory loss, involving primarily the lower limbs Posterior cerebral artery occlusion - Contralateral homonymous hemianopia with macular sparing = Visual agnosia Basilar artery occlusion = Locked-in $ > body and most of the facial muscles are paralyzed but consciousness remoins and the ability to perform certain eye movements is preserved Motorcontrol _Touchand pressure Body awareness Speech — Language Frontal lobe — reading CD Pariewal be a Di tempera tobe sie Zo Vision eZ Lhoséipitat be Ss Oicerebetum Hemineglect © pH > parietal lobe, contralateral Hemineglect = A fecture of parietal lobe lesion -> Contralateral + NN Nor-dominant hemisphere, Neglect - Patient is inattentive to one half of his visual field - _ €g. failing to eat food on the neglected side, might shave or opply makeup on to the non-neglected side Patient bumping into things on the right side + cerebellar symptoms > Rt hemianopia indicating Posterior circulation stroke F__PLABverse | win plabrersecomNeurology Cerebral arteries Cerebral arteries Middle cerebral artery (MCA) + On inates from the internal Carotid artery ‘+ Part of the anterior cerebral circulation ‘+ Supplies majority of the lateral surface of the hemisphere and temporal pole of the brain * Occlusion of MCA or it’s branches results in contralateral hemiplegia, hemianaesthesia and dysarthria due to facial weakness ‘+ MCA stroke involving Broca’s or Wernicke’s area would greatly affect speech ‘+ Homononymous hemianoy cerebralartery ‘can also occur but less commonly compared to occlusion of the posterior Anterior cerebral artery (ACA) ‘© Originates from the internal carotid artery ‘+ Supplies the frontal, parietal and cingulate cortex ‘+ Strokes involving the anterior cerebral artery is relatively rare * Occlusion of ACA results in motor deficits of the contralateral lower limb anda lesser degree paresis of the contralateral arm + Urinary incontinence and altered psychiatric status (e.g. memory impairments and emotional changes) can also occur Posterior cerebral artery (PCA) ‘© Originates from the basilar artery ‘© One of the major parts it supplies is the occipital lobe ‘© Amongst other symptoms, occlusion of PCA can result in homonymous hemianopia PLABverse | wn plabersecom 6Neurology Bell's palsy Risk factors * Pregnancy Other causes of facial weakness * om = Lyme disease > Travel Hx + Borrelia + URTIs antivodees ard vzantivodtes oe = Ramsay-Hunt $ > Unilateral facial weakness + gar pain + rash, ‘+ Unilateral facial weakness; facial droop © Drooling © Difficulty in eye closure ‘Pain around the ear may present during early days. © Less common <15 years old = Brain tumors-> MRI Treatment * Within 72 hours onset > Prednisolone (safe in pregnancy), high dose for 10 days *Ifsuspecting Ramsay-Hunt syndrome > Acyclovir + Eye protection with eye patch Which side of the face is affected by Bells’ palsy in the picture? ~The right side (right CN7), he’s trying to smile and only his left facial muscles are working ¢ \ If the patient is able to close his eves and raise his eyebrow on the affected side > UMNL (Central), not Bell's (see P.32) Trigeminal neuralgia Presentation ‘© Unilateral, shooting or stabbing electric shock-like facial pain ‘* Pain exacerbated with -> movement or touch especially in the jaw (2° and 3 branch distribution) ‘© Abrupt in onset and termination Diagnosis © Clinical diagnosis ‘+ MRlis routinely done to rule out other pathology (i.e. schwannoma, meningioma) Treatment ‘© Medications first then surgery ‘© Carbamazepine (Tegretol) > lamotrigine / phenytoin / gabapentin / botulinum toxin ‘© Surgical > Microvascular decompression Atypical facial pain = Chronic dull aching pain, poorly localized but located in the maxilla, + Could be unilateral or bilateral Herpes zoster ophthalmicus = Reactivation of varicella zoster virus in the area supplied by the ophthalmic branch of the trigeminal nerve + Features > vesicular rash around the eye, which may or may not involve the eye itself F__PLABverse | win plabrersecomNeurology Types of traumatic brain injury TTC Associated with skull fractures and MMA injury ‘© Usually a young athlete with an injury to the side of the head ‘Features of increased ICP © Immediate LOC then recovers spontaneously by lucid intervals, ©The patient will have adeciine ‘of mental function Lucid intervals (patient goes back to doing what he was doing before, before falling unconscious again) Investigation © CT/MRI > Bi-convex (see P.37) Management © Refer to. aneurosurgeon © Burr hole over pterion (the region where frontal, parietal, temporal end sphenoid bone Join together) to ensure that bleeding escapes instead if expanding intracranially * Followed by craniotomy and evacustion of hematoma If small volume hematoma with minimal midline shift and a good GCS without focal deficit > managed conservatively (e.. Mannitol) + serial CT scans to. monitor progress PLABVerse | wow plobversecom BT Teil Chronic (2-3 weeks) © Usually elderly on anticoagulation, high INR or alcoholic History of falls or minor head injury + Due to tear of Bridging veins ‘+ Slow onset of symptoms compared to epidural hematoma © Symptoms > progressive headache, confusion, nausea, vomiting or gradually evolving neurological deficits Acute (3-7 days) © Haslucid intervals > difficult to differentiate © Patient is barely awake during the lucid intervals © Think bigger trauma and sicker patient + Lowscs + Signs ofincreased IcP: = Headache, nausea, vomiting = Confusion = Pupils doesn’t respond to light - Decreased mental abilities = Shallow breathing = Seizures Investigations © CT/MRI> Crescent shaped (see P.37) Management © Surgical evacuation ‘* Mannitol, can be given with signs of ICP ST eae MCL ‘¢ Aneurysm formation is the most common etiology ‘© Sudden onset in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injury © Association with: - _PKD (Berry aneurysms) = Ehlers Danlos $ = Hypertension - Alcohol consumption © Hallmark > THUNDECLAP HEADACHE, very severe OCCIPITAL headache ‘© First headache in a long time in aperson who doesn’t usually suffer from headache, described as the worst headache by the patient ‘© Meningeal irritation (neck stiffness, photophobia, vorniting) Investi ‘© CT brain without contrast © Lumbar puncture = Only done if CTis inconclusive + no contraindications = Done after 12h from headache onset, to allow breakdown of RBCs - CSF > bloody then xanthochromic (bilirubin) After subarachnoid hemorrhage is confirmed, its origin needs to be determined > Cerebral angiography or CT angiography ‘Management after SAH > see p.40Neurology Generalized vs partial seizures obec ‘Means that electrical activity is limited to one * Loss of consciousness cerebral hemisphere © Both halves of the body (right and left) are ‘+ May or may not have LOC depending if they're involved simple or complex = Simple > conscious = Complex > not conscious Tonic - stiffness Clonic > twitches Tonic-clonic > stiffness + twitches Myoclonic Rapid jerking/twitching, can be experienced by a normal person while falling asleep Conscious + less than Status epilepticus > Aseizure lasting >5 minutes OR not regaining consciousness in the interictal period (between seizures) Management ABC High-flow oxygen | Seizures lasting longer than 5 minutes Yes No IV access —- Buccal midazolam pa (Or rectal diazepam) Seizure continues [scare continues Buccal midazolam Lorazepam iv (Or rectal diazepam) Phenytoin IV or Phenobarbital IV + Administer a maximum of 2 doses of the frst line treatment, if not resolved > IV Phenytoin - lV Phenytoinis preferred over IV Phenoberbital ~ Rectal diazepam is preferred over buccal Midazolam ~> due its availability and lower cost + Inchildren > Buccal midazolam is 1° line, if not available > rectal diazepam is used ~ _Ifseitures continue despite medications (>30min) > refer to the ICU for intubation - For home treatment > Rectal diazepam or buccal midazolam F__PLABverse | win plabrersecomNeurology Absence seizure Presentation Child usually <10 years old Loss of awareness (“daydreaming”), stare blankly into space, will not respond to their surroundings Face often looks pale with a blank expression May be accompanied by upturning of eyes or eyelids may flutter They would still be able to maintain the balance and do not fall during the episode Will return to normal a tired Seizures start and finish abruptly Occasionally, head may fall down a little, or arms may shake once or twice No photosensitivity Maybe triggered by hyperventilation ies after sei re (unaware of the seizure) but may not perform well and feel Diagnosis EEG Check FBC, glucose levels, ECG, MRI for other underlying causes Treatment Ifrecurring > Sodium valproate or Ethosuximide Epilepsy vs NEAD > Patients with NEAD usually retain consciousness, i > Video EEG is used to diagnose NEAD > Tilttable testing is used to diagnose vasovagal episodes jou elevated their arm above their face and drop it, the patient would avoid hitting his face Epilepsy > At east 2 unprovoked ‘epileptic seizures occurring 924h apart Epilepsy and pregnancy + Sodium valproate should NOT be used unless there’s no effective alternative Safest medications > Lamotrigine (1* choice), carbamazepine, levetiracetam ‘Woman on sodium valproate are advised to take effective contraception as itis highly teratogenic High dose (Smg) folic acid is recommended for at least 1 month periconceptually and throughout the first trimester Ifa patient on Sodium valproate wants to be pregnant ~_ If there was NO seizure for more than 2 years > Stop sodium valproate - Ifthe last seizure within less than 2 years > change to Lamotrigine If she became pregnant while on Sodium valproate ~ IF no seizure in last 2 years > Stop valproate and give folic acid 5mg for 12 weeks - ifthe last seizure was less than 2 years > Continue sodium valproate and give folic acid for 12 weeks In established pregnancy, changes to alternate antiepileptic drug therapy should NOT be undertaken solely to reduce teratogenic risk for 2 reasons: 1. Changing AEDs may precipitate seizures 2. Overlapping AEDs during the change exposes the fetus to effects of an additional antiepileptic drugs ‘Once an unplanned pregnancy is discovered it is usually too late for changes to be made to the epilepsy treatment regimen. The risk of harm to the mother and fetus from convulsive seizures outweighs the risk of continued therapy PLABVerse | wow plobversecom 10Neurology lepsy vs Non-epileptic attack disorder (NEAD) no resistance to opening it Symptom Epilepsy NEAD . iid History © Genetic factor eed physical or sexval abuse + Many including sleep deprivation, alcohol, ‘Triggers * Stress, panic flashing lights, sudden ® noises Occurin company | * Noasscciation + common Onset: * Sudden © Gradual coo 5 Oe © Often longer than 2 minutes (sometimes hours) Pelvic thrusting © Rare © Occasional * often dosed + Typically, open + Ifeyes are closed, there's Eyes / mouth © Ifeyes are closed, they have resistance to trying to open it + Rare * Common ‘Asynchronous * Rare common movements Tongue biting + common + Rare Incontinence + common + Rare Self-injury during * common + Rare attack Coie aie te © Rare Common attack © Apneic © Continuous + Common + Rare Post-ictal FEG «Slow Normal © Not responsive to multiple Medications © Responsive to medications B oh drug trials F__PLABverse | win plabrersecom 1Neurology Delirium > It can be classified asa clinical syndrome involving acute brain dysfunction or failure where there’s involvement of thought, perception and level of ewareness Precipitating factors + Metabolic derangement + Hypoxia + Infection + elrium > Acute onset : + Dementia > Chronidecine of mental functions Detaraticn + Schizophrenia > affects ounepeoole, dagnased © Aging after 6 months of having symptoms * Constipation * Medication (e.g, Benzodiazepines) Presentation © Acute onset ‘© Fluctuating leve's of consciousness + Disorientation, mood changes, paranoia = Memory impairment * Withdrawn or heightened arousal Diagnosis ‘© Clinical assessment via DSM-V © Consider radiological imaging to rule out organic pathology. Treatment 1" line > De-escalation techniques If failed > Olanzapine or Haloperidol for 1 week © UTIsare a common cause of delirium in the eigerty + Hospitalized old patient present with delirium > perform urine microscopy, culture & sensitivity :on's > Lorazepam ‘© Confusion & hallucinations after heavy drinking | ¢ Hallucinations after heavy drinking stops >48-72h ‘© Appears suddenly within 12-24h after heavy * Doesn't appear suddenly drinking ‘© More serious ‘+ Less serious diagnosis + Can be fatal when untreated ‘+ Amuch better prognosis than DTs Normal pressure hydrocephalus > Areversible cause of dementia seen in elderly, thought to be 2" to reduced CSF absorption at the arachnoid vil Presentation [GDU > grandpa in Arobic] - Hakim’s triad © Gait abnormaitties (may be similar to Parkinson's disease) > Early + Dementia ‘+ Urinary incontinence > as the awareness of urine passage is absent Investigation ‘© CT/MRIbrain > enlarged lateral and third ventricles ‘+ Lumbar infusion test (intrathecal infusion test) Treatment ‘© CSF shunting: ventriculoperitoneal, ventriculo-pleural, or ventriculo-atrial F__PLABverse | win plabrersecom 12Neurology Alzheimer Alsheimor' dizease (2) > The most common cause of Dementia + Aprasia (can’t move) prementariony Inabiity to carry out purposeful movements sh Elderly = 65 years + Aphasia (can’t speak) ° cary + Loss ofablity to speak ~ Memory loss (recent -> distant) + Agnosia can't recognize) ~ bifficuty finding words ose of ablity to recognize Followed by sates anos ~ Progressive language deficits - = Inability to make decisions Healthy Severs = Confusion Brain Alzheimer’s © Late ~ Disoriented My = Behavioral change =a 2 + Hallucinations Dingnodi 2 ‘© MRI brain > diffuse cortical atrophy ‘* Hexamethyiprpyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT), to differentiate Alzheimer irom Pick’s cisease and other pathology ‘* Mini-mental state exam (Folstein test), to assess the severity of cognitive dysfunctions and when to start medication Treatment = Acetylcholinesterase int ~ Doneperil [Dementia = Donepezil] - Galantamine [Donca is galavanting near the rive for @ meme) - Rivastigmine ‘* Memantine > 2 ine or in severe cases, contraindicated in depression itors > 1 line, notused in bradycardia, heart block, B-blockers or amiodarone ‘© Memory changes before personality ‘Personality changes before memory + Characterized by disinhibition- may be impulsive and disinhibited, with sexually inappropriate behaviors © Younger than Alzheimer’s (30-65y) ‘©The most likely affected anatomical structure is the orbitofrontal lobe ‘© Risk factors include HTN and DM * Treated by Trazodone, SSRls, if sexually disinhibited > Cimetidine or spironolactone © History of a cardiovascular event * DU Mini-mental state exam, used to indicate the presence of cognitive impairment = 25-30/30 > normal - 21-24/30> mild - 10-20/30 > moderate - <10/30 > severe impairment F__PLABverse | win plabrersecom 13Neurology Dementia, pseudodementia and grief response + Decline in memory and cognitive function sufficient to disrupt deily life Severe depression that presents with poor memory and concentration and impaired functional capacity Seen in elderly patients Hard to define as everyone is different Follows a tragic event (loss of a + Ifasked questions, ‘would give wrong, answers > This is because true dementia has poor attention and concentration Ifasked 2 question, would reply with “I don’t know, | can't be bothered, it's too difficult” > This is because they're often upset but their attention and concentration are often intact Response to antidepressant medication in le activities in an alert whereby they exhibit ae symptoms consistent with Usually < dementia but the cause is. sually <6 months actually depression + Onset relatively abrupt, + Poor memory © Often with past history of Goes through © Gradual onset depression stages of grief + Rarely reversible | » often short Angry, gullt, disbelief, tearful, difficulty steeping ‘Symptoms: reduce in intensity with acceptance of loss and readjustment Alzheimer’s patient doesn’t seek medical advice on his own, as he’s not aware of the condition F__PLABverse | win plabrersecom 14Neurology Meniere's disease Presentation ‘* Deafness, vertigo, tinnitus (DVT) + increased feeling of pressure in the ear ‘© Note: Vertigo ~ is usually the prominent symptom ‘© Episodes last minutes to hours © MRIis normal ‘+ Usually a female > male; 20-60 years old ‘© Typically, symptoms are unilateral but bilateral symptoms may develop after a number of years Treatment ‘© Acute attacks > buccal or intramuscular Prochlorperazine (-zine), Cyclizine ‘* Admission is sometimes required Vestibular schwannoma (Acoustic neuroma) -> high frequency SNHL, MRI is diagnostic, will have CN involvement Meniere’s disease -> low frequency SNHL Benign paroxysmal positional vertigo (BPPV) ‘One of the most common causes of vertigo Characterized by sudden onset of vertigo triggered by a change in head position Caused by dislodgement of tiny calcium carbonate crystals (otoconia) which migrate into the semi-circular canal (most commonly the posterior portion) Presentation ‘© Canbe preceded by infections 30 on turning over in bed, lying down, or sitting up from supine position (described as room's spinning) ‘© Each episode typically lasts 10-20 seconds vv a ‘© There’s nausea during episodes ~ Bppv > ists econ Diagnosis + Vestbular neuritis > lasts hours days ‘+ Hallpike's maneuver positive Treatment ‘+ Mostly spontaneous resolution with exacerbations [ ravers p> ererisaaLevo wea | + Epley’s maneuver ~ _ Arepositioning technique used to repesition otoliths back into the utricles from the posterior semicircular canals Dropattacks > Unexplained falls with no prodrome > Nolioss of consciousness and rapid recovery > Incidence increases with age Causes ‘* Vertebrobasilar insufficiency (due to decreased blood flow in the posterior circulation of the brain) © Weak legs (e.g. cauda equina $) Stokes Adams -> Unconscious + abnormal ECG Hypoglycemia > Unconscious + sweating Vasovagal syncope = Young woman + Unconscious + Emotional stress/pain/excitement/prolonged standing = Management > Reassure and tilt teble training F__ PLABverse | win plabrersecom 15Comparison of headaches Neurology BUC lat Deu Pe Tartar © Unilateral > 60-70% location Bilateral Strictly unitateral * Bilateral Veriable (sharp, burning or throbbing) Focused Pain on aay * TOBbIng/pulsating swiden sane character lghtening/pressing/Cull | | agua onset ee resolution Triggered by: stress, alcohol and exercise Pain intesity © Mild-moderate © Moderate-severe Very severe + Photophopia + Phonophopia Ipsilateral autonomic + Nausea “ features like: onus = Red/watery eye Aura = Constricted pupil Other ~ _Hefllache begins before = Unitateral facial © None aura ends or withinan symptoms ‘aura ends or within an sweating hour of the end hour of the end = Drooping eyelid - oe = Rhinorrhea Means Recurrence affect the (fortification spectra) eee = Ipsilateral parasthesia ~ _Ipsiateral weakness Around 30 mins 15mins-3h Duration continuously,canbe — * 4-72h May occur from 4 time longer every2-8 days Patient © Prefersto sit ina dark, q Restless and agitated # Able to do daily activity appearance room during an attack 0; 100% for 10-20mins © Aspirin © Triptan (oral) Subcut, or nasal triptans Management * NSAIDs © NSAIDs (aspiri Refers to a specialist if Paracetamol * Paracetamol the 1" bout of attack as may need neuroimaging © Propanolol > 1* line * Topiramate Prophylaxis | * Acupuncture Verapamil a Bu © Ifnot effective > Gabapentin P or acupuncture F__PLABverse | win plabrersecom 16Neurology Idiopathic intracranial hypertension © Asyndrome with increased intracranial pressure without evidence of a mass or hydrocephalus ‘* Its also known as pseudotumor cerebri and formerly benign intracranial hypertension. It is classically seen in obese women in child bearing age Presentation + Throbbing headache - worse in the morning + Headache exacerbated on bending or straining and relieved on standing up + Bilateral papilledema ‘+ Visual disturbances > Blurring of vision, flashes and ‘greying out’ on bending or straining © Gradual visual loss ‘+ Nausea and vomiting Investigations + Provided the worrying finding of bilateral papilledema, the primary concern is excluding a focal pathology such ‘as amass lesion ¢ MRI with contrast and MR venogram are the investigations of choice ‘© ACTscan and CT venogram are viable alternatives if MRI is unavailable. CT and MRI scans would be normal © Once a structural lesion has been excluded, the next step is a lumbar puncture. A high opening pressure indicates that the patient most likely has idiopathic intracranial hypertension. The fluid collected must also be sent for routine investigations such as microscopy, protein, and glucose. The CSF sample may also be examined for xanthochromia if a diagnosis of subarachnoid hemorrhage is being considered ‘© Additionally, visual field charting and intracranial pressure monitoring may be performed Management = Weight reduction ‘+ Stopping the causative drugm ‘+ Acetazolamide or other diuretics ‘© Serial lumbar punctures + Prednisolone Surgical intervention > Optic nerve sheath decompression and CSF shunting Migraine vs Idiopathic intracranial hypertension ‘© Typically unilateral ‘© Daily headaches ‘© Usually moderate to severe ‘© Usually mild to moderate (may present for © May have aura > auras are sensory ‘weeks to months) disturbances such as visual © Bilateral disturbances (flickering lights, spots, Visual symptoms including loss of vision partial loss of vision), numbness, which can last a few seconds & visual blurring, speech disturbances which occur ‘© Papilledema before OR during the headache ‘+ Worse in the morning © Better on standing ‘+ Aggravated by coughing or straining F__PLABverse | win plabrersecom 7Neurology Muscle syndromes Guillain-Barre syndrome | Myasthenia Gravis wetnene Weakness Yes Yes Yes Reflexes Absent or diminished Present Fatigue No Yes No Pain Often No No Fasciculations No No Yes Motor neuron disease (MND) > Acondition where motor nerves become damaged and eventually stop working -> muscle weakness The most common type, 8/10 MND patients ‘Symptoms tend to start in the hands and feet Muscles tend to become stiff and weak at first 2/10 MND patients Muscles first affected: muscles for talking, chewing and swallowing (the bulbar muscles) Uncommon Muscles of hands and feet are usually affected first but are not stiff Rare Muscles of leg are affected first Clumsiness in the hands and speech problems may develop Amyotrophic lateral sclerosis (ALS) Presentation ‘* Progressive weakness of bulbar (9,10,11,12), limb, thoracic and abdominal muscles ‘© Sensory, sexual and cognitive functions are intact ‘+ Limb-onset ALS > starts in the hands or feet © Bulbar-onset ALS > initial symptoms are difficulty speaking and swallowing ‘+ Hoffman's sign positive > indicates UMNL. Treatment * = Mor ‘© Neuroprotective medications ~> Riluzole Medications to treat respiratory symptoms, drooling, insomnia, fatigue and physiological symptoms Genetic testing and counseling for family For long-term feeding > Percutaneous endoscopic gastrostomy “VF __PLABverse | [Link] 18Neurology Guillain-Barre syndrome > Adisorder causing demyelination of the peripheral nerves > Usually preceded by infection (GI or respiratory infection) days-weeks prior Presentation © Weakness - Ascending pattern of symmetric weakness - Level of maximum severity of 2 weeks after initial onset - Facial weakness, dysphagia or dysarthria = _ Insevere cases > Respiratory failure -> FVC should be done to assess the need for ventilation © Pain = Neuropathic pain, particularly in the legs ‘© Hyporeflexia © sensory - _ Paresthesia and sensory loss, starting in the lower extremities Diagnosis ‘+ Nerve conduction studies -> Confirms diagnosis © Lumbar puncture - Elevated CSF protein without elevated cell counts (LP is not specific for GBS) = Elevated protein may not be found early and persists 1-2 weeks after the onset of weakness ‘+ Spirometry > most important test in acute setting as it determines the need for ICU admission & intubation Treatment ‘= IMIG or plasma exchange ‘* Ifo response in 2 weeks > consider repeating IVIG course or plasma exchange ‘* Treat neuropathic pain with gabapentin © Consider referral to ICU if respiratory depression detected > intubation and ventilation Syringomyelia © Arare condition where fluid-filled tubular cyst (syrinx) within the central, usually cervical spinal cord ‘* Symptoms and signs: - Neuropathic pain in the upper limbs exacerbated by exertion or coughing - _ Initially > Spinothalamic tract involvement > sensory loss of pain and temperature — may lead to painless upper 1b burns = orticospinal tract involvement > muscle weakness, starts in hands then forearms and shoulders > Partial paralysis of the LL ~ Loss of light touch, vibration and position senses in the feet - Loss of tendon reflexes F__PLAaBverse | wow plabversecom 19Neurology Syringobulbia ‘+ Occurs when the syrinx extends into the brainstem ‘* Syringomyelia + involvement of CNs (facial polsies) Myasthenia gravis - Diplopia = Brooping eyelids - Dysphagia = Dysarthria = Dysphonia Diagnosed by serum skeletal muscle nicotinic acetylcholine receptor antibody Lambert-Eaton $ Presentation © Young, female patients; mostly autoimmune ‘* Proximal weakness at the pelvic girdle / shoulder girdle ‘* Weakness improves with exercise as well a reflexes ‘© Cranial nerve involvement: dysphagia, dysarthria, ptosis, diplopia ‘© Associated with ScLc Diagnosis ‘© EMG > decreased amplitude in CMAP after single supramaximal stimulus but increases after exercise ‘+ Tensilon test (Edrophonium test) > may be positive but not as prominent as in myasthenia gravis ‘© Look for tumor > CT/MRI of chest, abdomen, pelvis + tumor markers Treatment © Treat tumor— first line ‘* Consider Methylpred one and IVIG Note that Tensilon test isn’t routinely done any longer Myasthenia gravis = Has fatique symptoms (2.9. walking > voice faded) + Associated with thyrotoxicosis = Intact reflexes Lambert-Eaton $ = Muscle function improves with use = Associated with SCLC = Absent reflexes scuc S> SIADH > Cushing $ 1 > Lambert-Eaton $ C Central tumor treated with chemo Bulbar palsy > LMNL, I, X, XI, Kil nerve palsies, dysphagia, dysarthria, dysphonia (nasal speech) tongue fasciculations Pseudobulbar > UMNL F__PLABverse | win plabrersecom 20Neurology Multiple Sclerosis > A demyelinating disease in which the insulating covers of central nerve cells in the brain and spinal cord are damaged > Mean age of onset > 30 years * Most patients follow a relapsing-remitting course > Optic neuritis + UMIN features 1. Transverse myelitis = Weakness, sensory symptoms = Urinary urgency and retention = Flexor spasms + Spastic quadriparesis or paraparesis, 2. Brainstem = Ataxia = Diplopia = Dysarthria + MS Autoimmune demyelination of CNS and spinal cord + Facial numbness ‘+ GBS > immune mediates demyelination of peripheralnen ous = Ophthalmoplegia system triggered by an infection = Gaze palsy 3. Cerebellum - Ataxia = Dysarthria = Nystagmus ‘© PLAB 1 stem usually have some clue to optic neuritis. Optic neuritis is on acute, sometimes painful, reduction or loss of vision in one eye and is a relatively common presenting symptom of MS ‘© Color vision may be impaired © Also, depression is common ‘* Pattern is usually relapsing-remitting: symptoms evolve over days, plateau, then resolves over doys/weeks Diagnosis © Mostly a clinical diagnosis ‘+ MRI (definitive diagnostic test) > demye occurring at multiple sites) + CSF Oligoclonal bands 10 NOT give NSAIDs for neuropathicpain-> it would mask the diagnosis Treatment ‘* Forrelapses > IV or oral Methylprednisolone * Fordisease modifying: - Dimethyl fumarate = Alemtuzumab and Natalizumab - _Interferon-beta or Glatiramer ‘* Symptom control: = Spasticity > baclofen or gabapentin = Tremors > botulinum Toxin = Fatigue > amantadine min D is usually given 1n and/or lesions disseminated in time and place (i.e. F__PLABverse | win plabrersecom aNeurology Parkinsonism This is the extrapyramidal triad of: 1. Tremor > worse at rest; often ‘pill-rolling’ of thumb over fingers 3 2. Hypertonia > rigidity + tremor gives ‘cogwheelrigicity’ felt by the examiner during rapid pronation/supination KA 3. Bradykinesia > slow toinitiate movement; actions slow and decrease in amplitude 7 with repetition: » = Decreased blink rate = Micrographia - Gait isfestinant (shuffling, pitched forward, shown in image) with decreased arm swing and freezing at obstacles or doors (due to poor simultaneous motor and cognitive function) - Expressionless face Parkinson’s disease (PD) © Due to loss of dopaminergic neurons in the substantia nigra, associated with Lewy bodies in the basal ganglia, brain- stem, and cortex © Mean age at onset is 60yrs ‘© Prevalence increases with age: 3.5% at 85-89yrs, ‘* Signs are invariably worse on one side—if symmetrical look for other causes Features © The parkinsonian triad ‘* Plus non-motor symptoms such as: = Autonomic dysfunction (postural hypotension, constipation, urinary frequency/urgency, dribbling of saliva) - Sleep disturbance - Reduced sense of smell = Neuropsychiatric complications, such as depression, dementia, and psychosis, are common and debilitating Investigations © Mainly clinical ‘© Aclinical response to dopaminergic therapy is supportive ‘© MRito rule out structural pathology ‘+ Functional neuroimaging (DaTscanTM, PET) is playing an emerging role Treatment ‘© Focuses on symptom control and does not slow disease progression '* Deep brain stimulation (DBS, may help those who are partly dopamine-responsive) ‘© Surgical ablation of overactive basal ganglia circuits (e.g. subthalamic nuclel) How to differentiate between side effects of Parkinson's vs medications (e.g. levodopa, dopamine agonists)? ‘+ More bradykinesia (‘less’ movements), rigidity and resting tremors ‘© Changes are gradual over the span of months/years ‘© Dyskinesias (‘extra’ movements) ‘+ Impulsive control disorder (e.g. excessive gambling, shopping) © Effects emerge after commencing medications + PLABVerse | wow plobversecom 22Neurology Notes about the medications for Parkinson's disease + Medication to treat Parkinson's > Levodopa, dopamine agonists (Ropinirole, pramipexole) ‘* Levoddopa and carbidopa is a common combination used in the management of Parkinson's disease * The rationale behind this combination is that carbidopa will inhibit the peripheral conversion of levodopa o dopamine. Dopamine does not cross the blood-brain barrier while levodopa does. The combination may be referred to as co-careldopa or byits trade name Sinemet® + One of the more common side effects of Levodopa (Sinemet) > Hallucinations > decrease the dose, that’s why it should always be started at a small dose and increased according to the patient’s response ‘* Sudden withdrawal of Levodopa may cause acute akinesia and neuroleptic malignant $ ‘+ AParkinson’s’ patient with nocturnal or early morning hypokinesia and rigidity > Controlled release preparations of levodopa (SR version) ‘Medication to treat tremors and dystonia in Parkinson's > Benzhexol ‘+ Medication to treat psychosis in an old Parkinson's patient > Lorazepam, lamotrigine Safe medications in Parkinson's Domperidone (prolongs QT interval}, '* Ondansetron (constipation effects are not great for the elderly) = Cydizine ‘+ Levomepromazine (for metaboli¢ cause} Avoid: Metoclopramide, Cinnarizine and Prochlorperazine (May Cause Parkinsonism) Lorazepam ‘* Clonazepam © Quetiapine (for longer-term, bya specialist) '* Clozapine (for longer-term, by a specialist) Avoid: Haloperidol, risperidone and olanzapine id: Pseudoephedrine and ephedrine if taking MAO-B inhibitors (e.g. 'SSRI (loss of libido common) ‘TCA (useful if also drooling owing to the side effect of dry mouth) Rivastigmine © Memantine “F__ PLABverse | www-piabversecom 23Neurology Parkinson’s plus syndromes Progressive supranuclear palsy > A degenerative disease involving the gradual deterioration and death of specific volumes of the brain Features ‘© Axial rigidity (axial trunk and neck are more affected than the limbs) © Falls (usually falls backwards while walking) © Dysarthria © Dysphagia ‘© Supranuclear gaze palsy affecting downgaze than upgaze > most distinctive feature ‘+ Symptoms of frontal lobe dementia > behaviors and personality changes Investigation Rl Gen en ed © Downgaze affected ‘© Tendency to fall backwards ‘© More progressive than Parkinson's ica «© Upgaze affected | Tendency to fall forward Shy-Drager $ (Multiple system atrophy) © Parkinson's symptoms (rigidity > tremor} ‘* Autonomic symptoms (urine incontinence/retention, erectile dysfunction, postural hypotension) Cortico-basal degeneration (CBD) © Akinetic rigidity involving one limb, + Cortical sensory loss (eg astereognosis) © Apraxia (even autonomous interfering activity by affected limb—the ‘alien limb’ phenomenon) FP __ PLABverse | [Link] 24Neurology Lewy body dementia Lewy body dementia is a neurodegenerative disease related to Parkinson disease Typically, patients would have memory loss, fluctuating cognitive impairment with visual hallucinations Concurrent parkinsonian symptoms such as rigidity, shuffling to walk and difficulty initiating movements may be present Typical presentation Dementia is usually the presenting feature, with memory loss and decline in problem-solving abilities Fluctuating levels of awareness and attention with nocturnal confusion Signs of mild Parkinsonism (tremor, rigidity, poverty of facial expression, shuffling gait, difficulty initiating movements) Visual hallucinations (animals or humans) > this is particularly important to differentiate Lewy body from other types of dementia in the exam Dementia precedes the Parkinsonism signs (eg. memory loss and. cognitive decline first and several months later develop tremor, rigidity and shuffling gait) ‘+ Sometimes, dementia and movement disorders present within 12 months from each other of which we would still cal this "Lewy body dementia" 1s seen if parkinsonism signs develop first, followed by memory loss and cognitive decline more than 12 months later Investigations MRI brain > Helpful to rule out other reasons for dementia but there are no easy distinguishable features to specifically diagnose Lewy body dementia ‘SPECT (single-photon emission computed tomography) > Useful after an MRI to show reduced dopar transporter uptake in the basal ganglia which is indicative of Lewy body dementia > This test is also known as the DatSCAN Management + Antiparkinsonian medications PLABVerse | wow plobversecom 25Neurology Myofascial pain syndrome Chronic pain disorder characterized by regional muscle pain associated with restricted painful regions or trigger points, pain is aching and deep in nature Occurs after a muscle has been contracted repeti Pai is relieved by changing position Mostly affected muscles: trapezius, levator scapula, infre-spinatus and scalenes ly (2.g. a long car ride) Cervical spondylosis Chronic cervical disc degeneration with disc herniation, calcification and osteophyteic outgrowths Early > Headach in the back of the head and pain in flexing neck Later > Radiculopathies due to root compression in arms and hands Examination > decrease in neck mobility (ROM) Essential tremors Symptoms Distal symmetrical postural tremor of the upper limbs Initially transient. May progress to become persistent ‘Amplitude of tremor may depend on physiological or emotional state May be seen to improve following alcohol ingestion ‘Tremors persist even when the patient is distracted Absent at rest Management + Propranolol -> 1” line ‘* Abrupt onset, spontaneous remission + stops when distracted + worsen when stressed + “pin rolling” tremors present at rest + rigidity (cogwhee!) + bradykinesia + postural inability ‘+ Intentional tremors, occur during voluntary active movements of an upper body, not present at rest '* Tremors would worsen when it approachesits target, usually include ‘overshooting or undershooting the target “Dysmetria” + Exemple: a patient would find difficulty due to his tremor when asked to touch his nose ‘© Typical dancing movement PLABverse | wn plabersecom 26Neurology Neurofibromatosis ‘* Autosomal dominant -> type 1 (Ch 17), type 2 (Ch 22), Schwannomatosis (benign nerve sheath tumor) More commen form © Café-au-lait spots Axillary or groin freckles: Peripheral neurofibromas Iris hamartomas (Lisch nodules) Scoliosis Association with pheochromocytomas Neurofibromatosis Type 1 (NF1) Neurofibromatosis Type 2 (NF2) cua signs “F_ PLABverse | [Link] 7Neurology Cauda equina syndrome ‘© Compression of the cauda equina is a surgical emergency ‘+ Symptoms of sciatica plus the following: - Saddle paresthesia = Urinary retention > urine accumulates until bladder is full > overtiow incontinence = Fecal incontinence required > Once diagnosed > urgent surgical decompression, to prevent irreversible loss to the sphincter and motor functions Red flags for low back pain - Age >50 years or <18 years = Unexplained weight loss >10kg within 6 months Night pain or pain at rest - Pain persists for >6 weeks = Failure to improve with therapy - History of cancer = Urinary incontinence or retention ~ Fecal incontinence - Saddle onesthesia/paresthesia - Progressive neurologic deficit = Vertebral tenderness Chemo MAN Cleplatin and Carboplatin * ototoxicty # nephrotoxicity Vincristine « peripheral neuropathy Bleomyein and Bue « pulmonary fibrosis ‘Trastuzumab and Doxorubicin * cardiotoxicity Cyclophosphamide # hemorrhagic cystitis Methotrexate, 5-FU, and 6-MP myelosuppression Note the following - Vincristine SE > peripheral neuropathy, felt as numbness and tingling “glove-and-stock distribution” with sensory loss and hypersensitivity and in some cases, motor and autonomic dysfunction - Other chemotherapy drugs that can cause peripheral neuropathy: Cisplatin, carboplatin, taxanes F__PLABverse | win plabrersecom 28Neurology Meningitis Features ‘* Headache + Fever +Photophobia + Vomiting + Neck stiffness ‘Meningocouzal sepsis > meningism ‘© Cranial palsies: CN Il, 1V, VI, Vil (eye movement & Facial n.) 41 8P, non-blanching petectial rsh Most common causative organisms of bacterial meningitis ‘© Neisseria meningitidis (meningococcus) > leading infectious cause of death in early childhood ‘+ Streptococcus pneumoniae (pneumococcus) > gram #ve organism + usually affects adults ‘* Haemophilus influenzae type b (Hib) ‘+ Streptococcus agalactiae (Group B streptococcus) and [Link] > most common cause in neonates Investigations ‘+ IFRASH > perform blood culture > Meningococcal septicemia (caused by Neisseria meningitides) ‘¢ IFNO rash +NO signs of increased ICP > perform Lumbar Puncture Eeeerel a = low © Normal © low © high © Normal or high + high ‘* Mainly neutropt Neutrophils, then lymphocytes oe | © Progresses rapidly + ‘* Increased lymphocytes Less severe than ° Geir signs of septic shock bacterial ‘© Cloudy/turbid/purulent © Clear + Fibrinweb ~ Bacteria eats glucose and shits protein > TE or bacterial = Lymphocytosis > Viral or T8 > glucose will differ Treatment ‘+ Antibiotics > should be Started before CT or LP whether it’s viral, bacterial or TB - Prehospital (Ambulance ora GP setting) > IV or IM Benzyipenicillin - Hospital setting > 1V Cefotaxime or IV ceftriaxone (Cephalosporin antibiotics) ‘* Ifraised ICP > summon help immediately and inform ICU (Mannitol} If symptoms of meningism > Dexamethasone IV Ampicillin/Amoxicillin + Gentamicin ‘Chloramphenicol ‘Oral Ciprofloxacin (1* line} or Rifampicin ‘Amphotericin B + flucytosine WV ceftriaxone + IV Amoxicillin s © Hearingloss ~ Hearing test should be performed after recovery - Meningitis can lead to hearing loss in acute and severe cases, Otitis media can lead to Meningitis ‘+ Hyponatremia (due to SIADH) restriction may be required * Complete recovery is the MOST LIKELY OUTCOME with a full treatment regimen PLABverse | wun plabrersecom 29Neurology Idiopathic intracranial hypertension > Idiopathic intracranial hypertension is a syndrome with increased intracranial pressure without evidence of a mass or hydrocephalus. It isalso known as pseudotumor cerebri and former'y benign intracranial hypertension > Itisclassically seen in obese women in child bearing age > Common associations include Cushing’s syndrome, hypoparathyroi 1m, iron deficiency anaemia, and thyroid disorders. Among the culprit drugs causing the condition is isotretinoin Features ‘© Throbbing headache - worse in the morning - Headache exacerbated on bending or straining - Relieved on standing up, ‘© Bilateral papilledema ‘© Visual disturbances -> Blurring of vision, flashes and ‘greying out’ on bending or straining, ‘+ Gradual visual loss ‘+ Nausea & vomiting Investigations ‘* Provided the worrying finding of bilateral papilledema, the primary concern is excluding a focal pathology such as a mass lesion ‘+ MRIwith contrast and MR venogram are the investigations of choice ‘© ACTscan and CT venogram are viable alternatives if MRI is unavailable. CT and MRI scans would be normal © Once a structural lesion has been excluded > next step is a lumbar puncture = Ahigh opening pressure indicates that the patient most likely has idiopathic intracranial hypertension The fluid collected must also be sent for routine investigations such as microscopy, protein, and glucose - The CSF sample may also be examined for xanthochromia if a diagnosis of subarachnoid haemorrhage is being considered ‘© Adgitionally, visual field charting and intracranial pressure monitoring may be performed Management © Weight reduction + Stopping the causative drug ‘+ Acetazolamide or other diuretics ‘¢ Serial lumbar punctures ‘© Prednisolone Surgical intervention -> Optic nerve sheath decompression and CSF shunting Papilloedema > Papilledema is optic disc swelling caused by increased intracranial pressure Causes © Brain tumour Idiopathic intracranial hypertension Cerebral venous sinus thrombosis © intracranial haemorthage Diagnosis Diagnosis papilloedema may be difficult © There are other differentials of optic disc swelling which look similar to papilloedema. These include: Optic neuritis, Ischaemia F__PLABverse | win plabrersecom 30Neurology Cavernous sinus thrombosis Presentation ‘© Headache —can be severe in intensity * Chemosis (edema of conjunctiva), edematous ioc eyelids, proptosis, painful ophthalmoplegia mates \ + Fever cutis nicrw ‘* Usually preceded by sinusitis Aten Me e8 0 ANN Diagnosis seaerteorss \ © CT/MRI venography . Treatment © Referral to neurosurgery \ © Antibiotics © Anticoagulation (e.g. heparin) © +/- Corticosteroids and surgical drainage Restless leg syndrome (Willis-Ekbom $) Features © Urge to move (usually legs) ‘+ Abnormal sensation, tingling or pain ‘+ Tends to appear in the evening leading to sleep disturbance ‘* Worsened by > Pregnancy © Relieved by > Moving ‘* Associated with Lewy Body Dementia Investigations ‘© Serum iron > usually associated with IDA (if serum ferritin is low > add iron supplementation despite normal Hb) Management ‘+ Avoid alcohol, smoking and caffeine along with exercise and good sleep hygiene ‘= Drugs needed in 20%: - Dopamine agonist (2.8. Ropinirole), as dopomine is responsible for regulating body movements = Gabapentin = Pregabalin Cerebral abscess Features ‘* Headache > most common symptoms ond is often on the same side of abscess © Fever ‘© Focal neurological deficit + Corobral abscess shows many ofthe features of brain + Earpain & discharge tumors as both are spaceoccupying lesions + Changein mental state Rae abaideeelyi * Grand mal seizures Brain abscess > CT ‘* Nausea, vomiting and neck stiffness ‘© Papilledema > due to cerebral edema * CT scan > sadiolucent space-occupying lesion (ring enhancing lesion) F__PLABverse | win plabrersecom 31