CP - Acute Onset Paraparesis

7/30/2019 CP - Acute Onset Paraparesis

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Acute Onset Paraparesis:Acute Onset Paraparesis:

A Case StudyA Case Study

R NarismuluGreys Hospital

February 2008


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HistoryHistoryz Patient BZ

z

39 old malez Presented with sudden onset bilateral lower

limb paralysis

z Associated numbness and paraesthesiainvolving both limbs

z Associated urinary retention

z No faecal incontinence, but did complain ofconstipation

z No other symptoms


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z PMH: Was admitted 1/52 prior to neurology

presentation at Northdale Hospital for a

diarrhoeal illness and was subsequently

discharged after 3 days.No other previous medical history

z PSH: Laparotomy 2004 aetiology unknown

z Medication: No chronic or currentmedication use.


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z Social History:

Resides in Mpomeni with his fiance andten year old daughter who are both well.

Previous smoker with a ten pack yearhistory.

Social alcohol intake.

z Family History: Non-contributory

z Allergies: nil


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Physical ExaminationPhysical Examination

z General Examination :Well looking patient with good hydration

Tinea capitis and Tinea pedis notedright posterior triangle and right

epitrochlear lymphadenopathy present

Melanonychia

No other clinical findings


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CVS Exam : BP 117/75 PR 87

JVP not elevated

AB undisplaced

Normal heart soundsNo murmurs

No carotid bruits

Respiratory Exam : Not distressed

Lung fields clear

No adventitious sounds


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Abdominal Examination : Laparotomy scarSoft

Non-tender

Hepatomegaly 3 cm

No splenomegaly

No ascites

Normal bowel sounds


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CNS ExaminationCNS Examination

z Higher function was intactz Right handed

z

No meningismz All cranial nerves intact

z No anatomical abnormalities of the spine

and skull


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Motor System Upper LimbsMotor System Upper Limbs

zTone, power and reflexes were normal in bothupper limbs.


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Motor System Lower LimbsMotor System Lower Limbs

z

Decreased tonezPower was zero

zAbsent reflexes

zDowngoing planters


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SensationSensation

PreservedPreservedProprioception

PreservedPreservedVibration

T12L1Light touch

T12L1Pinprick

LeftRight


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zSphincter tone was decreased

z

Decreased peri-anal sensationzAbdominal Reflexes absent

zPrimitive Reflexes absent

zNo clinical evidence of cerebellar disease

zThe patient was not ambulant


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AssessmentAssessment

z39 year old male

zRecent diarrhoeal illness

zClinical stigmata of RVD

zAcute onset flaccid paraparesis with bladder and

bowel involvement

zSensory level at L1 on the right and T12 on the left

zSparing of the dorsal columns

zFeatures in keeping with spinal shock


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Where is the lesion ?Where is the lesion ?

z Anterior aspect of the spinal cord betweenT12 and L1

z Parasagittal lesion


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Differential Diagnosis ofDifferential Diagnosis of

Acute Onset ParaparesisAcute Onset Paraparesis1)Extramedullary Lesions (Intra/Extra Dural)

Spinal trauma

Pathological fractures

Epidural abscess

Dural AVM

Bleeding into a mass lesion

2) Intramedullary lesions

See flow chart


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Differential Flow Chart in Acute OnsetDifferential Flow Chart in Acute OnsetParaparesis: Intramedullary CausesParaparesis: Intramedullary Causes

Intramedullary

Demyelinating Ischaemia Myelitis

Viral Bacterial Parasitic ParainfectionInfarction Haemorrhage

Trauma

Global Ischaemia

Thromboembolism

Vasculitis

MS ADEM


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InvestigationsInvestigations

z Blood investigations

z Structural imaging MRI spine

z CSF examination


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Blood InvestigationsBlood Investigations

4.81Folate

860Vit B12

19.4CRP

68ESR

125PLTS

38 %HCT

32.5MCH

94.8MCV13Hb

4.8WCCFBC


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190CK

0.68Mg

1.09PO4

2.39CaCPM

72Cr

2.2Urea

25.7HCO3

106Cl4.27K

134NaU/E


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N/RRPR

0.96TSH

4.6Glu

53ALT

99GGT

109ALP

1.8DBili

21Bili25Alb

76TPLFT


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posRVDVCTnegSPEP

negSACE

pendingCD4

negANF

negRFConnective Tissue Screen


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MRI: T1 Without GadoliniumMRI: T1 Without Gadolinium


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MRI: T2W clearMRI: T2W clear


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MRI:T1W With GadoliniumMRI:T1W With Gadolinium


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MRI FindingsMRI Findings

zT1 weighted hyperintensity at T11 indicatingoedema, inflammation and possibly haemorrhage

z T2 weighted lesion at T11 becomes hypotense,

hyperintensity extending longitudinally from T6 toT10

z T1 weighted with Gadolinium- slight

enhancement post gadolinium injection at the T11region.


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MRI Findings cont.MRI Findings cont.

z A final assessment of a longitudinalmyelitis extending from T6 T10 with a

possible haemorrhage at T11 localised to

the anterior aspect of the spinal cord wasmade.

z Suggestive of an anterior spinal cord infarct.


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CSF AnalysisCSF Analysis

NegFTA-Abs

NegNeurocytercicosis ELISANegNeurotropic Viruses

Neutrophils, histiocytesCytology

NegCLAT

2.8 BG 4.6Glucose

NegIndia Ink

0.44Protein0RBC

16 cmH20Opening Pressure

0Lymphs

2PolysCSF


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Working Diagnosis ofWorking Diagnosis ofIntramedullary Cord LesionIntramedullary Cord Lesion

z Myelitis with or without haemorrhage

z Anterior spinal artery infarct in the region

of T11

z Demyelinating disorder


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Differential Flow Chart in Acute OnsetDifferential Flow Chart in Acute OnsetParaparesis: Intramedullary CausesParaparesis: Intramedullary Causes

Intramedullary

Demyelinating Ischaemia Myelitis

Viral Bacterial Parasitic ParainfectionInfarction Haemorrhage

Trauma

Global Ischaemia

Thromboembolism

Vasculitis

MS ADEM


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Demyelinating Disorders: MSDemyelinating Disorders: MS

z Multiple Sclerosis (MS)1) Relapsing-remitting or progressive course

2) Pathological triad of i) CNS inflammation

ii) demyelination iii) gliosis

3) Autoimmune disease

4) Caucasian population


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Demyelinating Disorders: ADEMDemyelinating Disorders: ADEMz Acute Disseminated Encephalomyelitis

z

Antecedent immunisation- post vaccinalencephalomyelitis (rabies, influenza, DPT,hepatitis B etc)

z Antecedent infection- postinfectiousencephalomyelitis (measles, rubella,herpesviruses, influenza, mycoplasma)

z Immune response to myelin basic protein(MBP)


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ADEM continuedADEM continued

z Clinical features1) Rapid onset

2) Focal or multifocal neurological

dysfunction

3) Recent infection or immunisation

4) Monophasic course


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ADEM continuedADEM continued

z Pathology- perivascular inflammation anddemyelination

z Severe form of ADEM also known as acute

haemorrhagic leucoencephalitis results invasculitic and haemorrhagic lesions with a

devastating clinical course


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ADEM continuedADEM continuedz Diagnosis

1) History: recent immunisation or infection2) Physical exam: neurological deficit of rapid

onset

3) CSF: mildly elevated protein, lymphocyticpleocytosis, mixed polymorphonuclear-lymphocytic pattern in initial stages,

transient CSF oligoclonal banding (rare)4) MRI: gadolinium enhancement of white

matter in brain and spinal cord


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Viral Causes of MyelitisViral Causes of Myelitis

z Immunocompetent: HSV 2, VZV, EBV,rabies virus, polioviruses (now rare becauseof immunisation)

z Immunocompromised: CMV, HTLV1(Tropical Spastic Paraparesis)

z Chronic viral myelitis can be associated

with advanced HIV as well as HTLV1 onthe basis of a vacuolar myelopathy


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Bacterial Causes Of MyelitisBacterial Causes Of Myelitis

z Rarez Almost any pathogenic species

z Listeria monocytogenes most frequently

isolated


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Parasitic Causes of MyelitisParasitic Causes of Myelitis

z Toxoplasmosis: associated with HIVz Schistosomiasis: intensely inflammatory

and granulomatous myelitis secondary to a

tissue-digesting enzyme produced by theova


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Parainfectious MyelitisParainfectious Myelitis

zNon-specific immune mediatedinflammatory reaction related to infection of

any aetiology and occurring at any point

during the course of the illness.


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Spinal Cord InfarctionSpinal Cord Infarctionz Blood supplied to the spinal cord by a single

anterior spinal artery and paired posterior spinalarteries.

Causes of spinal cord infarction include:

z Traumatic: fracture dislocation of vertebrae oracute back trauma (embolism of nucleus

pulposus material into spinal vessels)

z Global Ischemia: e.g. shock, cardiorespiratoryarrest, aortic dissection


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Spinal Cord Infarction continuedSpinal Cord Infarction continued

zHaemorrhagic infarcts DIC and otherplatelet abnormalities or bleeding disorders

z Hypercoaguable states

z Endothelial abnormalities Vasculitis e.g.connective tissue diseases and HIV


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Spinal Cord Infarction continuedSpinal Cord Infarction continued

z Cardiogenic emboli

z Thromboembolism of any cause in arterial

feeders

z Surgical clipping of aortic aneurysms

z Pregnancy


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Main ConsiderationsMain Considerations

1) Para infectious MyelitisSupporting the diagnosis:

clinical presentation i.e. recent viral illness

and acute onset of symptoms

MRI findings suggestive


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2) Viral Myelitis HSV / CMVSupporting the diagnosis:

CMV initial presentation with GE

HSV commonly associated with HIV

Against the diagnosis

No suggestive skin lesions

Neurotropic viral screen negative


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3) Anterior Spinal Cord InfarctSupporting the diagnosis

Injury localised to a vascular territory

Haemorrhagic injury seen on MRI

Acute Onset


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4) ADEMSupporting the diagnosis:

clinical presentation i.e. recent viral illness

and acute onset of symptomsMRI findings suggestive

Against the diagnosis:

CSF findings

Lesion was localised


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ManagementManagement

z Mr BZ was managed for both ADEM and HSVmyelitis

z Acyclovir 750 mg tds ivi 10/7z Methylprednisolone 500mg od ivi 5/7

z Paracod 1g tds po

z Physiotherapy

z He will be followed up at the clinic in one monthto review outstanding results and to assess

progressz At time of discharge there was no improvement in

neurological deficit


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The EndThe End

Thank YouThank You

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CP - Acute Onset Paraparesis