Brainstem Stroke

8/3/2019 Brainstem Stroke

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CASE PRESENTATION

Dr Ayesha S KhanPGR-1


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PRESENTING COMPLAINTS

69 yr old male, known hypertensive anddiabetic, with no other co-morbiditiespresented to OPD with

Dysphagia 2 days Vertigo 2 days


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HOPI Pt was in his usual state of health 2 days back

when he suddenly started to have difficulty inswallowing his saliva while he was lying in hisbed. He tried to take sips of water but wasunable to swallow.

On getting up from his bed he experiencedsevere vertigo, with a feeling of environmentspinning which lasted for about 5-10mins.

No h/o fall, loss of conciousness, loss of speech,fits, nausea, vomiting or motor or sensory loss. No h/o diplopia, loss of vision or facial weakness


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Pt was taken to the Services hosp

immediately where his CT scan was donewhich showed Senile cerebral & cerebellar atrophy,

lacunar infarct in left frontal lobe Films were not present.


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He was managed conservatively there, buthis symptoms persisted. Attendants tooksecond opinion from Dr Attiq ur Rehmanwho adviced admission in MMW of FMH.

No h/o similar event in past. Patient also c/o relative constipation forlast 4 days.

No h/o fever, cough, burning micturition,any incontinence. No other systemiccomplaint


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PAST HISTORY

HTN 40yrs (On Blockium 50mg BID) DM- 15yr ( On Glucophage and Dianil)

No h/o IHD, TB or COPD. No other previous medical/surgical history.


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EXAMINATION

A middle aged man sitting comfortably onthe bed with NGT in place. Appears in nodistress.

BP : 160/80mmHg , no postural drop

Pulse: 84/min, good volume, regular Afebrile O2 Sat : 98% at room air


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GPE

Pallor-ve, Jaundice-ve, Edema-ve,Cyanosis-ve, Clubbing-ve.

Well hydrated.


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CNS EXAMINATION GCS: 15/15 Well oriented in time place and person Higher mental status intact

Cranial Nerves: No facial muscle weakness Rt sided Miosis Rt sided partial ptosis Absent Gag reflex Nasal twang +ve Tongue movements normal


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Cerebellum: Nystagmus ve Gait normal

Dysdiadokokinesia normal Heel shin test normal Rhomberg sign normal


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Musculoskeletal : Power : 5/5 bilateral for both limbs.

Sensations: Rt: Normal for both UL & LL Lt: Decreased for UL & LL Deep Tendon Reflexes : Sluggish

Plantars : Non specific


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SYSTEMIC EXAMINATION

CVS : S1+S2+0 RESP: NVB+0

GI : Soft, non tender, no visceromegaly,BS normal


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Assessment

Brainstem ischemia (Lateral MedullarySyndrome, TIA)

Benign paroxysmal positional vertigo Meniers disease Otitis media Vestibular Schwannoma Cerebellar infarction Multiple sclerosis


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PLAN MRI Brain Lipid Profile CBC, RFTs, LFTs Echocardiography, ECG and carotid doppler.

BSL x TDS Started : G-Pride 4mg 1xOD Blockium 50mg 1xOD

Loprin 150mg 1xODLipiget 10mg 1xHSSyp Duphalac 2 TSF x HS


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LABS

TLC : 10.2 Hb : 15.1 Platelets: 270

Urea: 29 S/Creat : 1.1 S/ Uric acid: 3.9

Urine exam: Normal Al phos: 227 SGOT: 23

SGPT: 27 STB: 0.9 Cholesterol: 243

TG: 174 HDL: 38 LDL: 171


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Carotid Doppler: Bilateral plaques in

carotid vessels,

more on the rightside whichcomparativelycompromised bloodflow in rt sidedvertebral arterialsystem.

MRI Brain: Cerebral atrophy.

Bilateral

periventricularsmall vesselischemicdisease,demyelination involvingcorona radiatabilaterally.


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Progress of the Patient

Patient stayed in MMW for 3 days and hissymptoms of loss of pain and temperaturesenses on the left trunk and extremitieswere relieved. Gag also became positiveafter 3 days, though sluggish.

He was discharged on 23.11.11 on themedications mentioned before and wasasked to follow up in Neuro OPD.


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Brain stem stroke syndromes It is a condition involving a stroke of the brain

stem. Because of their location, they ofteninvolve impairment both of the cranial nuclei andof the long tracts.

Types include: Lateral Medullary Syndrome Medial Medullary Syndrome Lateral Pontine Syndrome

Medial Pontine Syndrome Millard Gubbler Syndrome Benedicts Syndrome Webers Syndrome


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Lateral medullary syndrome

Lateral medullarysyndrome (Wallenberg syndrome and posterior inferior cerebellarartery syndrome ) is a disease in whichthe patient has a constellation ofneurologic symptoms due to injury to the

lateral part of the medulla in the brain,resulting in tissue ischemia and necrosis.


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Signs and symptoms This syndrome is characterized by sensory deficits

affecting the trunk and extremities on the opposite sideof the infarction and sensory deficits affecting the faceand cranial nerves on the same side with the infarct.Specifically, there is a loss of pain and temperaturesensation on the contralateral side of the bodyand ipsilateral side of the face. This crossed finding isdiagnostic for the syndrome.

Clinical symptoms include Swallowing difficulty, or dysphagia Slurred speech

Ataxia Facial pain Vertigo, nystagmus Horner syndrome Diplopia

palatal myoclonus.


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FEATURESVestibular Nuclei Vestibular

system: vomiting, vertigo, nystagmus

Inferior cerebellar peduncle Ipsilateral cerebellar signs including ataxia,dysmetria (past pointing), dysdiadokokinesia

Central tegmental tract Palatal myoclonus

Lateral spinothalamic tract contralateral deficits in pain and temperature

sensation from body (limbs and torso)

Spinal trigeminal nuclei & tract ipsilateral loss of pain, and temperaturesensation from face

Nucleus ambigous (vagus n. &

glossopharyngeal n.

ipsilateral laryngeal, pharyngeal, and palatal

hemiparalysis:dysphagia, hoarseness,diminished gag reflex (efferent limb - CN.X)

descending sympathetic fibers ipsilateral Horner's syndrome (ptosis, miosis,& anhydrosis


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Cause

Occlusion of the posterior inferior cerebellarartery (PICA) or one of its branches or ofthe vertebral artery, in which the lateral part of

the medulla oblongata infarcts, resulting in atypical pattern. The most commonly affected artery is the

vertebral artery, followed by the PICA, superiormiddle and inferior medullary arteries.


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Treatment Involves focusing on relief of symptoms and active

rehabilitation to help those suffering from the strokesyndrome recover their activities of daily living and copewith neurologic loss that can be psychologicallydevastating.

Depressed mood and withdrawal from society can beseen in patients following the initial neurologic insult.

Treatment for this disease can be disconcerting becausesome individuals will always have residual symptomsdue to the severity of the blockage.

Two patients may present with the same initialsymptoms right after the stroke has occurred, but afterseveral months one patient may fully recover while theother is still severely handicapped.


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Treatment Feeding Tube :

A feeding tube inserted through the mouthor gastrostomy may be necessary if swallowing isimpaired

Speech Therapy : Speech therapy may be beneficial in dietrecommendations and helping to understand if thereis risk for aspiration pneumonia.

Pain Relief : Medication may be used to reduce or eliminate pain.

Some studies have reported success in mitigating thechronic neuropathic pain associated with thesyndrome with anti-epileptics such as gabapentin


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Treatment

Long term treatment Involves the use of blood thinners

like warfarin.

Patients will often remain on thesemedications or an aspirin regimen for the restof their lives in order to minimize the risk ofanother stroke.

Other medications may be necessary in orderto suppress high BP and risk factorsassociated with strokes.


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Prognosis

Depends upon the size and location of thearea of the brain stem damaged by thestroke. Some individuals may see adecrease in their symptoms within weeksor months. Others may be left withsignificant neurological disabilities for

years after the initial symptoms appeared


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Medial Medullary Syndrome

Most frequently results from the occlusionof the Vertebral Artery or Anterior Spinal artery


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Presentation

Lesion of Hypoglossal nerve: Ipsilateral paralysis of half the tongue and atrphy.

Tongue deviated toward the side of the lesion uponprotrusion

Lesion of Medial Leminiscus: Contralateral Deficit of proprioception and touch,

pressure and vibratory sensations in the limbs and

body Lesion of Corticospinal Tract:

Contralateral spastic hemiparesis of both limbs.


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Lateral Pontine Syndrome

Results from the occlusion of Anterior inferior cerebellar artery or Superior Cerebellar artery


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Presentation Inferior Cerebellar Peduncle:

Ipsilateral limb ataxia

Spinal V: Ipsilateral pain & temperature loss of face

Spinothalamic tract: Contralateral pain and temperature loss of the body

Decending Hypothalamics: Ipsilateral Horner sydrome

Fibers of 7th

nerve: Ipsilateral facial palsy Fibers of 8 th nerve:

Hearing loss


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Presentation

This produces ipsilateral horizontal gaze palsy -> PPRF facial nerve palsy -> 6 th nerve contralateral hemiparesis -> CS tract hemisensory loss -> Medial leminiscus internuclear ophthalmoplegia ->Medial

Longitudinal fasiculus


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Millard-Gubler syndrome

Millard-Gubler syndrome is a lesion ofthe pons


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Presentation

Symptoms result from the functional loss ofseveral anatomical structures of the pons,including the

6th and 7th cranial nerves Fibers of the corticospinal tract.

It is a form of "crossed hemiplegia," as theparalysis of muscles controlled by the facialnerve occurs on the same side as the lesion,while the hemiplagia of muscles below the neckoccurs on the opposite side as the lesion.


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Benedikt syndrome

Benedikt syndrome , or paramedianmidbrain syndrome , is a rare type ofposterior circulation stroke of the brain,with a range of neurological symptomsaffecting the midbrain , cerebellum andother related structures.


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Characterization CN III oculomotor nerve palsy Cerebellar ataxia including tremor.

Neuroanatomical structures affected include CNIII nucleus Red nucleus, Corticospinal tracts Cerebellum.

It is very similar to Weber's syndrome; the main difference between thetwo being that Weber's is more associated with hemiplegia (i.e.paralysis), and Benedikt's with hemiparesis (i.e. weakness).

Causes Benedikt syndrome is caused by a lesion ( infarction, hemorrhage,

tumor, or tuberculosis) in the tegmentum of the midbrain and cerebellum.Specifically, the median zone is impaired. It can result from occlusion ofthe posterior cerebral artery.

Treatment Deep brain stimulation may provide relief from some symptoms of

Benedikt syndrome, particularly the tremors associated with the disorder.


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Claude's syndrome

Claude's syndrome is characterized bythe presence of an oculomotor nervepalsy, contralateral hemiparesis,contralateral ataxia, andcontralateral hemiplegia of the lower face,tongue, and shoulder.


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Cause and presentation

Claude's syndrome is caused by midbrain infarction asa result of occlusion of a branch of the posteriorcerebral artery. This lesion is usually a unilateralinfarction of the red nucleus and cerebral peduncle,affecting several structures in the midbrain including:

Structure damaged Effect Dentatorubral fibers contralateral ataxia

Corticospinal tract fibers contralateral hemiparesis

Corticobulbar tract fibers contralateral hemiplegia of lower facial muscles,tongue, and shoulder

Oculomotor nerve fibers Ipsilateral oculomotor nerve palsy with adrooping eyelid and fixed wide pupil pointeddown and out; probable diplopia


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Weber's syndrome

Weber's syndrome (Medial MidbrainSyndrome)

Oculomotor nerve palsy and Contralateral hemiparesis or hemiplegia


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Presentation

Structuresdamaged Effect

Substantia Nigra contralateral parkinsonism because itsdopaminergic projections to the basalganglia innervate the ipsilateral hemispheremotor field, leading to a movement disorder of thecontralateral body

Corticospinal fibers contralateral hemiparesis and typical upper motorneuron findings

Corticobulbar tract difficulty with contralateral lower facial musclesand hypoglossal nerve functions

Oculomotor nervefibers

ipsilateral oculomotor nerve palsy with a droopingeyelid and fixed wide pupil pointed down and out.This leads to diplopia

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Brainstem Stroke