بسم ال الرحمن الرحيمCVA

Academic group OF internal medicine

- Revision note of CVA- 2010Dr. Mohamed Eisam Elhag Mahmoud

MBBS, Alneelain University Faculty of Medicine

Note: Dr. Mohammed Isam Al-Hajj does not have any financial relationships to disclose nor will he discuss any non-approved drug or device uses.

# Personal History:

• -name• -age : usually in elderlly but there is some

cases in young!!• Q-causes of CVA in young?• A.V.M• CVS disease => embolism , A.F , post MI• Premature atherosclerosis• Arterial Disection

• Therombophilia • Antiphospholipid “anticardiolipin syndrome”• Vasculitis , SLE• Bleeding disordor• Berry aneursm

• -sex. – residance . –tribe . –occupation . – marital state

• * Pt. is Rt. / or Left handed => “ dominant hemisphere”

• - D.O.A:- pt. admitted at twinty second of / /2010.

• # C/O: Rt. Side weakness , which preceded by numbness.

#HPI:- “ pridiposing Factors must mention at first”

• If the => pt. is known case of:-• 1- HTN for 5 yr , recived captopril&not on

regular ttt.• 2- DM for 7 yrs ,on oral hypoglycemic

agent but not on regular medication.• 3- Mitral stenosis for 4 yrs, not recived

digoxine.

• The condition started 1 day P.T.A by weakness which is:-

• Onset: • Sudden -> Embolism “with maximum intensity at

the begin”• Rapid-> Therombosis”pt.weak up from sleep then

after few hours develop weakness “ • Drammatic-> Haemorrhage “when pt. do his

ordinary activity”

• Gradual -> SOL “focal lesion then>>>-progress”

• Intermittent -> multiple sclerosis “ scatterd in place ,time & disease . may in young , ex. Pt. blind >>>then monoplegia.

• Trauma !!

• 2- The condition ass\not ass with Coma => cortical lesion

• 3- The weakness ass\not ass with sign of incrase ICP =>SOL “headach, convulsion , loss of consciousness”

• 4- The weakness ass\not ass with Fever & Convulsion=> absccess & granuloma

• 5- The weakness ass\not ass with Sphintric disturbance=> anterior cerebral artery.

• 6- The weakness ass\not ass with Cranial nerves disturbance “ especially 7th => mouth devation”

• -7th C.N palsy + weakness at same side -> un-crossed hemiplegia “ at level of cerebral cortex”

• - 7th C.N palsy + weakness at opposite side=> crossed hemiplegia” at the level of Brain stem”

7- The weakness ass\not ass with Speech disturbance => cortical lesion.

Aphasia• Sensory: can talk but can not

understand.=fluent=receptive, ask him to follow your command?ex. touch your right ear with left hand?

• Motor: can understand but can not talk.= nonfluent=expressive. Ask him to till you the pen parts? ( most common “Brocas aphasia”

• Global: sensory + motor

• Dysphasia => cortex• Dysartheria => internal capsule , Brain stem

, may cerebllum, basal ganglia, Tongue ex. Aphthous ulcer. ( slurred,staccato,scanning)

• Dysphonia: volume of speech=> vocal cord:- innervation, candida,papilloma.

• THEN , complete the CNS analysis:-• - SENSORY => no/ there parathesia , numbness,

….• - remaining of cranial nerves: • Normal smelling, no visual disturbance, no double

vision , no affection of eyes movment, difficult in mastication,affect of face sensation, jaw hang, deviation of mouth, accumulation of food ,loss of hearing, balance disturbanc , change in voice, difficult in swalowing, no diffecult in speech, can rise his shoulder, rotate his neck.

• Degree of disability: cant walk, walk with asscistance.

• Cerebellar sign

# systemic review:

• CVS: valvular lesion => shooting embolus. (no chest pain , no palpatation “imp. Negative”). MI->shooting thrombus.

• RS: TB => tubercloma act as SOL.• GIT: espcially Diarrhea -> dhydation->>thrombotic state.• Renal : polycystic kidney->ass e sacular aneyrsum->may

rupture “ Haemorrage”• Skin: any skin rash or Bleeding=>bleeding tendancy

“haeg.”• Gynoclogical: menarch,menopause , amount => increase

bleeding tendancy.

# PMH:-• T.I.A : transient neurological deficit”ischemic”,

with complete recovery within 24h.• R.I.N.D : reversible ischemic neurological

deficit”=>recovery from 24h---7days.• Simillar condition. *causes of recurrent stroke?

Multiple sclerosis, CVS disease not treated well,bleeding tendancy.

• No DM , no HTN • TB, syphilis => act as SOL.• Hospitilization & blood tranfusion->

(HIV,Toxoplasma,1ry CNS lymphoma).

• #FH: DM, HTN, simillar condition->PKD, familial hyperlipidemia, bleeding tendancy.

• #Drug history:• Not known to be sensitive to any medication

known to him/her including pencillin.• On regular medication: oral contraceptive=>

increase viscosity of blood->> thrombotic.

• Antiplatelet ,anticoagulant,NSAID,steroid.

• # social history: housing condition , educational level,jop,health insurance, sibling =>(to know who is take care of pt.) ,bad habites->smooking,alcoholic. Classes(low/modrate/high)socioeconomic class.

• #summery:- 68yr old male , known case of HTN for 5 yrs not on regular medication, present with Rt. Side weakness, the condition ass with aphasia & loss of consciousness.

O/E:

• General: looks ill, lay flat, average wt.& height , not tachypnic or orthopnic, has NG-tube in his Rt. Nostril, canulated in Rt. Hand

• Vital signs: BP , PR ,RR , Temp.

Neurologically:

• Oriented in time,place &person• Memory for remote ,recent&immediate

events are intact.• In good mood , good bhaivours &

intelligent.• He suffer from motor aphasia

Cranial nerves examination ……..

• Motor System:-• Posture • Abnormal movment• Trophic change• Wasting

Motor examination

• Inspection• Tone• Power• Reflexes• Coordination

Tone: • Hypertonia “spastic” 1may be+clonus, if

hypotonia=>spinal shock.- Power : • determin grade of power. • examine each group” weakest”,- Reflexes: • deep-> tendon. • Superficial-> planter reflex , abdominal

reflex.

• # Sensory:- according to dermatome• 1-Superficial: touch, pin prick• 2- Deep : vibration, position sense.• 3- Cortical sensation: asterogenosis , tow points

discrimination , sensory intention, apraxia,graphesia.

if there any disturbance=> • Coordination• Gait : circumduction• Back examination.

• Then Examine: • CVS: for irregular irregular pulse-> Atrial

fibrillation• Pericardium ->underling valvular lesion.• Carotid pulse& carotid bruit.• Eyes: DM retinopathy, HTN retinopathy,

Arcus senile.• Examine other systems.

Q- How to investigate this pt?

• CT-scan : immediately done to role out haemorage, but infarction will visualize up to 12 h.

• MRI: gold stander investigation• Carotid Doppler: to show stenosis , if there

+ pt.=> for Endoarterectomy.• Investigation for underling causes: • Blood sugar, cholesterol level , Hb , • ECG, Echo. ,• ANA , Anti-DNA , Anti-thrombin III ,

Protein C & S , Urine.

Q- what are the risk factors for stroke?

1- Non – modifiable: • Age, gender “m>f “ , hereditary , previous

vascular events(MI – stroke – peripheral embolism).

2- Modifiable:• HTN , cigarette smoking , DM ,

Hyperlipidemia , HF , AF , alcoholic , + FH , oral pill , & polycythamia.

Q- What is your dignosis?

• CVA, Rt. Side hemiplegia due to left cortical lesion which result of Embolism from cardiac source “mitral stenosis complicated by atrial fibrillation “ associated with Rt. UMN Fascial Nerve palsy “ uncrossed hemiplegia” , pt. has motor aphasia, now pt. is improved slightly .

Q- where is the site of lesion?

A- Cortical: • Convulsion• Coma=> impair consciousness• Un-crossed hemiplegia -> power different• Homenumus hemnopia• Aphasia=> if lesion affect dominant

hemisphere• Absence of cortical sensation.

B- Internal capsule:• Deep hemiplegia • Deviation of mouth “uncrossed”• Dysphagia -> risk aspiration pneumonia• UMN Fascial palsy –same side• No convulsion, No coma, No aphasia, No

hemnumous heminopia.

• C- Brain stem:Symptoms • (4D)=> Dysartheria,Dysphonia,

Diplopia&Dysphagia. “ipsilateral C.N dysfunction”. 3RD C.N palsy, impair upgaze.

• Fascial palsy usually LMN• Crossed :• Contralateral spastic hemiparesis• Hyperreflexia & extensor plantar response

(UMN).• Contralateral hemisensory loss & ipsilateral

incoordination.

Q- what is the nature of lesion?

Haemorrage Infraction

embolism thrombosis

Dramatic onsetOccure when pt in his/her ordinary activity

Sudden onset with max. intensity at the begin

Rapid onset when pt. weak up from sleep then within hours weakness at maximum onset.

Also condition associated with:Vomiting Convulsion fever

Usually there is clear source of embolism. Ex.. cardiac -> preceded palpitation. Fat embolism ” bone fracture”. air embolism. pulmo. Embolism -> VSD “paradoxical embolism”

Source:. HF. MI

Q- What is the complications of stroke?

• 1- Chest infection. 2-Dhydration. 3- hyponatremia. 4-hypoxemia. 5- seizures.6- DVT & pulmonary embolism. 7-Frozen shoulder. 8-Bed sore. 9-urinary infection. 10- constipation. 11- psychological harmfull.•

Q- How to manage such pt.?• General :• Psychological support• Frequent change position to prevent bed

sore.• NG- Tube • Urinary catheterization.• Physiotherapy-> to prevent wasting &

contraction.• Specific: for underling cause

• Q- what are the poor prognostic factors of CVA?

• Elderly 2- co-morbid disease 3-re-infraction 4-haemorage inside infraction 5- coma 6-hypoxemia 7-hypercapnia 8-itrogenic->rapid decrease of high BP.

• Q- mention extracranial sites of thromboembolism?

• 1-carotid &its branches 70% . 2- heart 20% (AF) 3-5%different

• • Q- mention risk factors for haemorragic

stroke?• HTN, AVM , Bleeding disorders,

&anticoagulant ttt.

Q- What is Door needle time mean in treatment of stroke?

• If the pt. present within 1st 3 hour “befor cytotoxic oedema formation” We can give Thrombolysis after exclude haemorrage & We can give Asprin safty, the best thrombolytic is => t.PA ( S/E: increase haemorrage size)

• If the source of thrombosis:• Inside heart=> warferin• Outside heart=> asprin 300mg crushed immediately,

Endartrectomy => if carotid 70% occluded.

• Q- if the lesion? • In middle cerebral artery:- Weakness in arm &

face > leg.• In Anterior cerebral artery:- Weakness in leg >

arm & face.• Q- what is the prognosis of TIA? ( ROLE OF

30%)• 30% will develop nothing• 30% will develop TIA within 2 years• 30% will develop TIA within 6 month& 30% of

them will die•

Thank you for your attention

Now start of OSCE…..

www.smso.net

Best whishes

أليس الماضي و عبق التاريخ يا رمزالنضاللؤلؤة النيل حورية الضفاف باهية الجمالهواك يناديني فأهرع عبر المدائن والبوادي و التلل

BRAIN ABSCESS

EPIDURAL HEMATOMA

SUBDURAL HEMATOMA

•ASSESS GRADES OF BEST MOTOR RESPONSE (Max score 6)

• 6 Carrying out request ('obeying command') • 5 Localizing response to pain. • 4 Withdrawal to pain - pulls limb away from

painful stimulus. • 3 Flexor response to pain - pressure on nail bed

causes abnormal flexion of limbs • 2 Extensor posturing to pain - stimulus causes

limb extension • 1 No response to pain.

The Glasgow coma scale (GCS)

• ASSESS GRADES OF BEST VERBAL RESPONSE (Max score 5)

• 5 Oriented - patient knows who & where they are, and why, and the year, season & month.

• 4 Confused conversation - patient responds in conversational manner, with some disorientation and confusion.

• 3 Inappropriate speech - random or exclamatory speech, no conversational exchange.

• 2 Incomprehensible speech - no words uttered, only moaning. • 1 No verbal response. •

Cont

• EYE OPENING (Max score 4)• 4 Spontaneous eye opening. • 3 Eye opening in response to speech - that

is, any speech or shout. • 2 Eye opening in response to pain. • 1 No eye opening. • TOTAL SCORE ...... / 15 RECORD

YOUR FINDINGS You may record you findings on a specific ‘CNS’ chart. Otherwise record in the following fashion:

Conti

UMN Vs LMN

UMN – contralateral facial weakness with forehead sparing

LMN – ipsilateral facial weakness with no forehead sparing

Bell’s Palsy

Acute LMN nerve palsyUnilateral Inflamed facial nerve within petrous temporal

bone24 hx ear acheNo sensory loss Idiopathic?HSV – acyclovir – inconclusive evidence?short course high dose steroids

Worth learning a differential for facial weakness:

Acoustic neuromaBell’s PalsyMiddle ear infectionRamsay-Hunt syndromeParotid gland tumoursMumpsGuillain-BarreMononeuritis multiplexMSMND

What is this Condition?

Ramsay Hunt Syndrome

Cerebellar Examination

• Coordination• Intention Tremor• Finger nose test• Gait• Heel Knee Test• Dysdiadokokinesis• Nystagmus

Power Grading (Medical Research Council Scale)

0 No movement2 Flicker of movement3 Movement but not against gravity4 Movement against gravity but not

resistance5 Weak movement against resistance6 Normal

Upper motor neuron lesion

• Stroke (hemiplegia), cerebral palsy, MS (spastic paraplegia)

• No muscle wasting• Pyramidal weakness - Upper limb – weak abductors and extensors

(flexed)- Lower limb – weak adductors and flexors

(extension)- Increases tone (spasticity/ clasp knife)• Hyperreflexia and clonus. Upgoing plantar.• Circumductive gait

Peripheral neuropathy

• Usually generalised (diabetic), mononeuropathy (medicn nerve) or radiculopathy

• Distal sensory or motor and sensory loss • Inspection - Pes cavus, wasting, fasciculation,clawing• Tone – decreased• Power – distal weakness • Reflexes – Reduced/ absent• Sensory – glove and stocking loss / paraesthesia• Disease affecting pathology of the peripheral nerves may

be perfectly normal/ proximal weakness (Guillain- Barre syndrome)

• Eg Charcot- Marie-Tooth,

Retina

Optic Nerve

LGB

Optic radiation

Chiasma

Lower fibres(Temp lobe)

Upper fibres(ant parietal lobe)

Occipital Cortex

Retina

Optic Nerve

LGB

Optic radiation

Chiasma

Lower fibres(Temp lobe)

Upper fibres(ant parietal lobe)

Occipital Cortex

Retina

Optic Nerve

LGB

Optic radiation

Chiasma

Lower fibres(Temp lobe)

Upper fibres(ant parietal lobe)

Occipital Cortex

CN II:

Optic Nerve

Lateral GeniculateBody

Pretectal Nucleus

Edinger – WestphalNucleus of III

ConvergenceCentre

Cilliary Ganglion

Cilliary Body - Iris

Afferent Pathway Efferent Pathway

Extra Ocular Eye Muscles

Signs of right third nerve palsy

• Ptosis, mydriasis and cycloplegia

• Abduction in primary position

• Limited depression • Limited adduction

• Normal abduction

• Limited elevation

• Intorsion on attempted downgaze

Important causes of isolated third nerve palsyIdiopathic - about 25%

Vascular disease - hypertension, diabetes

Posterior communicating aneurysmTrauma

Extraduralhaematoma

Prolapsingtemporallobe

Edge oftentorium

Aneurysm

Chiasm

Third nerve

Posterior cerebralartery

Midbrainpushedacross

Horner’s Syndrome

PtosisMiosisAnhydrosisEnopthalmos

Lesion to cervical/sympathetic chainEXAMS: Horner’s syndrome = pancoast tumourBUT ptosis does not = horner’sCould be CN III lesion

Anatomy of fourth nerve

• Only cranial nerve to emerge dorsally• Crossed cranial nerve• Very long and slender

Internal carotid artery

Postr. communicating artery

IIIVI

Postr.cerebral arterySupr.cerebellar artery

Basilar arteryIV

Signs of right fourth nerve palsy

• Right overaction on left gaze

• Right underaction on depression in adduction • Vertical diplopia

• Right hyperdeviation in primary position when left eye fixating• Excyclotorsion

slightly upwards and outwards (extorsion)

Recent right sixth nerve palsy

Right esotropia in primary position due to unopposed action of right medial rectus

Marked limitation of right abduction due toright lateral rectus weakness

Hess chart of recent right sixth nerve palsy

• Contraction of right chart and expansion of left• Right chart - marked underaction of lateral rectus and mild overaction of medial rectus• Left chart - marked overaction of medial rectus

Left VI Nerve Palsy (lateral Rectus)

CN V: Trigeminal Nerve

Sensory Patient eyes closed Cotton wool Touch each division left and right Compare each side Corneal reflex – not normally done!

Motor Ask patient to clench teeth○ Temporalis○ masseter

Jaw jerk Not normally done! Checking for UMN lesion (brisk reflex)

CN VIII: Vestibulo-cochlear

• “noticed any change in hearing?”

• Hearing:– Block other ear

– Rubbing fingers together, see when they can no longer hear it

• Rinne’s – tuning fork louder in front or behind?

• Weber’s – is it louder in one ear?

CN IX: Glossopharyngeal

Sensory: post 1/3rd of tongue (facial nerve ant 2/3rd)

Motor: stylopharyngeusAutonomic: salivary glands Inspect:

Position of uvula“say aahh”

See if the uvula deviates to one side (away from abnormal side)

CN XI: Accessory Nerve

Inspect neck: Sternomastoid wasting/fasciculation Shoulders equal?

Put you hand on side of face and say “push against my hand”

Test each shoulder separately: Shrug your shoulder against my hand”

UMN: ipsilateral sternomastoid and contralateral trapezius wasting

LMN: ipsilateral sternomastoid and trapezius wasting

CN XII: Hypoglossal Nerve

• Inspect tongue (resting inside mouth)– Wasting, fasciculations

• Stick your tongue out:– Watch if is deviates to one side:

• Weakness on the side it deviates to

Representative of Case History #2

Guillain-Barré Syndrome (GBS)

•acute inflammatory demyelinating polyneuropathy

•disorder of the peripheral nerves

•attack of the myelin sheath of nerves by antibodies or white blood cells

•rapid onset of ascending paralysis

•begins with weakness and/or abnormal sensations of the legs and arms

•breathing muscles may be so weakened

•following gastrointestinal or respiratory viral infections

•palpitations (sensation of feeling heartbeat), difficulty beginning to urinate, incomplete bladder emptying, incontinence (leaking of urine), constipation, and muscle contractions

Representative of Case History #1

DUCHENNES MUSCULAR DYSTROPHY

Gower’s Sign

•marked enlargement of calves•hyperlordosois•decreased tendon reflexes•normal sensation

The end…..

• Thank You!!Thank You!!

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