Confidently diagnosing acute • Sudden onset: fine one moment…… • Rapid evolution of symptoms • Witness account: last seen well • Previous neurological illness Diagnostic difficulties

• That’s not what textbooks say! • Evolving stroke – fluctuating symptoms • Mostly -ve, but may have +ve symptoms • “Rapidly resolving” deficit may actually be evolving stroke • Dense weakness followed by apparent full resolution may still be stroke, not TIA • Strong denial by patient – rt hemispheric • Beware of “” Clinical patterns

• FAST +ve strokes • FAST –ve strokes

• Lacunar syndromes • Cortical stroke FAST –ve strokes

• Cerebellar strokes • Occipital infarcts • Non-dominant parietal lesions • Sensory strokes • Frontal/para-sagittal infarcts causing just leg weakness Chameleons

• Stroke in disguise • Evolves over time

• Clues: – Abrupt onset – Vascular risk factors – Focal deficit Chameleons

• Movement disorders: , hemichorea (subthalamic n, globus pallidus, connections)

• Confusion (temporal lobe, frontal, fluent , neglect, hemianopia)

• Limb pain (thalamus, lateral medullary infarct)

• Neglect, denial (Anton syndrome)

• Apathy/depression (bilateral thalamic lesions) Non-acute stroke presentations

• Stuttering/progressive hemiplegia • Progressive Basilar thrombosis • Confusion, falls, carpet burns • Patient having a stroke and refusing to accept it ! ‘Recrudescence of Deficits After Stroke’-Topcuoglu et al. • Data from 1700 patients • 164 episodes among 153 patients who had a diagnosis of (145 ischaemic and 8 haemorrhagic) • Motor-sensory or language function involvement.

1. Topcuoglu MA, Saka E, Silverman SB, Schwamm LH, Singhal AB. Recrudescence of Deficits After StrokeClinical and Imaging Phenotype, Triggers, and Risk Factors. JAMA Neurol. Published online August 07, 2017. doi:10.1001/jamaneurol.2017.1668 Patient cohort

• Compared with those patients on MGH stroke registry who did not have post stroke recrudescence those who did were more likely to be: – African American – Female • …and more likely to have had: – Severe neurological deficits at the time of stroke – Dyslipidaemia – Diabetes Infection P <0.001 Use of benzodiazepines P=0.02

Key triggers

Hypotension P=0.04 Hyponatraemia Insomnia and P=0.01 stress P=0.06 It’s all about connections

• Neuroplasticity Take home note

• Temporary exacerbation of previous neurological deficit (without fresh damage) is common • The clue is in the history-previous stroke and when • Ask about original symptoms and recovery • Ask about triggers that brought on new event • Consider all of these before re-scanning and re- admission • Counsel patients Amyloid Attacks

• Stereotyped, transient neurologic • Spread to contiguous parts 2- 10’ • May involve areas in several vascular territories. • ? small cortical petechial hg. focal . • Rate of spread similar to migraine ?? Spreading depression of neuronal activity. • Transient confusion, of visual misperceptions, chiro-oral paraesthesia • Diagnosis T2* MRI (gradient echo) Other mimics

• Peripheral n. compression, radicular or plexus injury • Transient Global Amnesia • Unexplained falls • Isolated vertigo • • Wernicke’s (diplopia,,confusion) • Hemi- • Bulbar MND Partial Seizures • Commonly young or middle aged adults. • Following previous cortical stroke. • May have antecedent symptoms. • Onset seconds-minutes. • Positive neurological symptoms. • March of symptoms • Resolution over few minutes. • ‘Epilepsia Partialis et Continua’ •  Amnesia for the event. • Stereotypical attacks, reduce with antiepileptic treatment. Seizures & Post-ictal paralysis

• May last up to 48 hrs • induced alteration in neuronal function • Residual neurology points to the epileptic focus • In up to 15% of the epileptics • Mono or hemiplegia • aphasia • gaze deviation • hemianopia • Seizure may be unwitnessed/undiagnosed • 1-2% strokes present with seizures But.

• 2% of patients have a seizure at stroke onset. • TACS & PICH / SAH. • 25% incidence in ICH/SAH. • 5% patients will have a seizure within the first two weeks post stroke. • Thrombolysis – ICH; Up to 36 hours. • EEG can be difficult to interpret.

Hypoglycaemia

• Adrenergic symptoms/signs may be absent • Patient may be alert or confused • Neuroglycopenia • Hemiplegia, quadreplegia, extensor plantar • Aphasia • Brainstem signs • Signs usually reverse after glucose – in minutes, but up to a few hours • Could lead to permanent neurological sequelae • May ‘re-express’ old stroke • Alcohol intoxication/alcoholics RavidJM: Transient insulin hypoglycemichemiplegias. Am J MedSci1928;175:756-759

Migraine forms.

• Hemiplegic Migraine. • Acephalgic Migraine. • ‘Benign recurrent vertigo’. • Prolonged Aura. • Status migrainosus. Migraine with/without aura

• 2.0-2.5 increase in stroke risk • Strokes can mimic migraine! • Neurological disturbance is almost always transient. • Stereotypical attacks • Neurological symptoms ‘march’: visual, hemisensory –cheiro-oral, dysarthria /aphasia, unilateral weakness Migraine aura.

• Gradual Onset. • Positive symptoms. • Symptom spread over several seconds to minutes. • Gradual resolution over 20-60 minutes • • Recurrent Stereotyped attacks. • Typically young. Hemiplegic Migraine

• Watch for the typical ‘march’ of symptoms • Usual duration of neurological symptoms is 30 minutes -2 hours • could be ipsilateral or contralateral • Hemiplegia may outlast headache • In the familial variety, neurological signs could become permanent • Frank hemiplegias • ataxia and other cerebellar signs • coma Mass lesions

6% present abruptly: • Haemorrhage • • Oedema • Ischaemia • Seizure Brain Tumours

• Can cause transient neurological symptoms lasting minutes or indeed permanent • There are symptoms which are acute by nature eg dysphasia, diplopia, dysphagia • Acute symptoms due to haemorrhage, hydrocephalus, oedema, seizure or Todd’s • On a non-contrast CT scan, metastasis and tumours can appear like infarcts • Symptoms due to oedema can resolve well with steroids (temporarily) 1 week of confusion, dysphasia, rt facial droop

Day 1 Day3 3 Day3 Day 10 CT

76 year old man with right hemispheric signs, with rapid development of delirium

Day 14 Subdural haematoma

• SDH’s can present with transient or permanent FAST +ve neurological deficits

• Up to a third of the chronic subdural haematomas could be a FAST +ve mimic Peripheral limb lesion

• Ulnar nerve lesion (elbow haematoma after fall), overuse of crutches • Radial nerve lesion • Arterial obstruction: acute onset of left arm weakness 0/5, severe ache, ice-cold. Patient was in AF Summary

• Diagnosis of hyper-acute stroke can be challenging • Evolving stroke may be punctuated with temporary return of movement • Dense deficit at any stage is more likely to be stroke than TIA, even if it seems to be rapidly improving • Dense weakness, especially of upper limb is more likely to be associated with large vessel occlusion Summary -2

• Rt hemispheric strokes may be more difficult to diagnose – weakness my be less marked, pt may deny deficit, executive function affected • Learn to look for ‘neglect’ • Aphasia may be misdiagnosed as confusion • Lacunar stroke affects 2 or more contiguous parts, never skip a region, do not cause language deficit Summary -3

• Monoplegia or part of a limb involvement almost always due to cortical stroke • Patients with migraine can have stroke, so do not start with bias • Hyper-acute stroke may cause +ve features • Not all strokes are FAST+ve • If in doubt, consider CT-angiogram to look for LAO, the worst type of stroke