acute onset paraparesis: a case study
TRANSCRIPT
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Acute Onset Paraparesis:Acute Onset Paraparesis:A Case StudyA Case Study
R NarismuluGreys HospitalFebruary 2008
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HistoryHistoryPatient BZ39 old malePresented with sudden onset bilateral lower limb paralysisAssociated numbness and paraesthesia involving both limbsAssociated urinary retentionNo faecal incontinence, but did complain of constipationNo other symptoms
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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
PSH: Laparotomy 2004 aetiology unknown
Medication: No chronic or current medication use.
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Social History: Resides in Mpomeni with his fiancée and ten year old daughter who are both well.Previous smoker with a ten pack year history.Social alcohol intake.
Family History: Non-contributory
Allergies: nil
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Physical ExaminationPhysical Examination
General Examination :Well looking patient with good hydrationTinea capitis and Tinea pedis notedright posterior triangle and right epitrochlear lymphadenopathy presentMelanonychiaNo other clinical findings
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CVS Exam : BP 117/75 PR 87JVP not elevatedAB undisplacedNormal heart soundsNo murmursNo carotid bruits
Respiratory Exam : Not distressedLung fields clearNo adventitious sounds
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Abdominal Examination : Laparotomy scarSoftNon-tenderHepatomegaly 3 cmNo splenomegalyNo ascitesNormal bowel sounds
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CNS ExaminationCNS Examination
Higher function was intactRight handed No meningismAll cranial nerves intactNo anatomical abnormalities of the spine and skull
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Motor System Upper LimbsMotor System Upper Limbs
Tone, power and reflexes were normal in both upper limbs.
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Motor System Lower LimbsMotor System Lower LimbsDecreased tone
Power was zero
Absent reflexes
Downgoing planters
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SensationSensation
PreservedPreservedProprioception
PreservedPreservedVibration
T12L1Light touch
T12L1Pinprick
LeftRight
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Sphincter tone was decreased
Decreased peri-anal sensation
Abdominal Reflexes – absent
Primitive Reflexes – absent
No clinical evidence of cerebellar disease
The patient was not ambulant
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AssessmentAssessment39 year old male
Recent diarrhoeal illness
Clinical stigmata of RVD
Acute onset flaccid paraparesis with bladder and
bowel involvement
Sensory level at L1 on the right and T12 on the left
Sparing of the dorsal columns
Features in keeping with spinal shock
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Where is the lesion ?Where is the lesion ?
Anterior aspect of the spinal cord between T12 and L1
Parasagittal lesion
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Differential Diagnosis of Differential Diagnosis of Acute Onset ParaparesisAcute Onset Paraparesis
1)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 Onset Differential Flow Chart in Acute Onset Paraparesis: 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
Blood investigations
Structural imaging – MRI spine
CSF examination
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Blood InvestigationsBlood Investigations
4.81Folate860Vit B1219.4CRP68ESR125PLTS38 %HCT32.5MCH94.8MCV13Hb4.8WCCFBC
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Blood InvestigationsBlood Investigations
190CK0.68Mg1.09PO42.39CaCPM72Cr2.2Urea25.7HCO3106Cl4.27K134NaU/E
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Blood InvestigationsBlood Investigations
N/RRPR0.96TSH4.6Glu53ALT99GGT109ALP1.8DBili21Bili25Alb76TPLFT
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Blood InvestigationsBlood Investigations
posRVDVCTnegSPEPnegSACE
pendingCD4
negANFnegRFConnective Tissue Screen
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MRI: T1 Without Gadolinium MRI: 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
T1 weighted – hyperintensity at T11 indicating oedema, inflammation and possibly haemorrhageT2 weighted – lesion at T11 becomes hypotense, hyperintensity extending longitudinally from T6 to T10T1 weighted with Gadolinium- slight enhancement post gadolinium injection at the T11 region.
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MRI Findings cont.MRI Findings cont.
A final assessment of a longitudinal myelitis extending from T6 – T10 with a possible haemorrhage at T11 localised to the anterior aspect of the spinal cord was made.Suggestive of an anterior spinal cord infarct.
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CSF AnalysisCSF Analysis
NegFTA-Abs
NegNeurocytercicosis ELISANegNeurotropic Viruses
Neutrophils, histiocytesCytologyNegCLAT
2.8 BG 4.6GlucoseNegIndia Ink
0.44Protein0RBC
16 cmH20Opening Pressure
0Lymphs2PolysCSF
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Working Diagnosis of Working Diagnosis of Intramedullary Cord LesionIntramedullary Cord Lesion
Myelitis with or without haemorrhage
Anterior spinal artery infarct in the region of T11
Demyelinating disorder
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Differential Flow Chart in Acute Onset Differential Flow Chart in Acute Onset Paraparesis: 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
Multiple Sclerosis (MS)1) Relapsing-remitting or progressive course2) Pathological triad of i) CNS inflammation
ii) demyelination iii) gliosis3) Autoimmune disease4) Caucasian population
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Demyelinating Disorders: ADEMDemyelinating Disorders: ADEM
Acute Disseminated EncephalomyelitisAntecedent immunisation- post vaccinalencephalomyelitis (rabies, influenza, DPT, hepatitis B etc)Antecedent infection- postinfectiousencephalomyelitis (measles, rubella, herpesviruses, influenza, mycoplasma)Immune response to myelin basic protein(MBP)
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ADEM continuedADEM continued
Clinical features1) Rapid onset2) Focal or multifocal neurological
dysfunction3) Recent infection or immunisation4) Monophasic course
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ADEM continuedADEM continued
Pathology- perivascular inflammation and demyelinationSevere form of ADEM also known as acute haemorrhagic leucoencephalitis results in vasculitic and haemorrhagic lesions with a devastating clinical course
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ADEM continuedADEM continuedDiagnosis
1) History: recent immunisation or infection2) Physical exam: neurological deficit of rapid
onset3) CSF: mildly elevated protein, lymphocytic
pleocytosis, 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
Immunocompetent: HSV 2, VZV, EBV, rabies virus, polioviruses (now rare because of immunisation)Immunocompromised: CMV, HTLV1 (Tropical Spastic Paraparesis)Chronic viral myelitis can be associated with advanced HIV as well as HTLV1 on the basis of a vacuolar myelopathy
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Bacterial Causes Of MyelitisBacterial Causes Of Myelitis
RareAlmost any pathogenic speciesListeria monocytogenes most frequently isolated
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Parasitic Causes of MyelitisParasitic Causes of Myelitis
Toxoplasmosis: associated with HIVSchistosomiasis: intensely inflammatory and granulomatous myelitis secondary to a tissue-digesting enzyme produced by the ova
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Parainfectious MyelitisParainfectious Myelitis
Non-specific immune mediated inflammatory 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 InfarctionBlood supplied to the spinal cord by a single anterior spinal artery and paired posterior spinal arteries.
Causes of spinal cord infarction include:
Traumatic: fracture dislocation of vertebrae or acute back trauma (embolism of nucleus pulposus material into spinal vessels)
Global Ischemia: e.g. shock, cardiorespiratory arrest, aortic dissection
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Spinal Cord Infarction continuedSpinal Cord Infarction continued
Haemorrhagic infarcts – DIC and other platelet abnormalities or bleeding disorders
Hypercoaguable states
Endothelial abnormalities – Vasculitis e.g. connective tissue diseases and HIV
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Spinal Cord Infarction continuedSpinal Cord Infarction continued
Cardiogenic emboli
Thromboembolism of any cause in arterial feeders
Surgical clipping of aortic aneurysms
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 symptomsMRI findings suggestive
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Main ConsiderationsMain Considerations
2) Viral Myelitis – HSV / CMVSupporting the diagnosis:CMV – initial presentation with GEHSV – commonly associated with HIVAgainst the diagnosisNo suggestive skin lesionsNeurotropic viral screen negative
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Main ConsiderationsMain Considerations
3) Anterior Spinal Cord InfarctSupporting the diagnosisInjury localised to a vascular territoryHaemorrhagic injury seen on MRIAcute Onset
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Main ConsiderationsMain Considerations
4) ADEM Supporting the diagnosis:clinical presentation i.e. recent viral illness and acute onset of symptomsMRI findings suggestiveAgainst the diagnosis:CSF findingsLesion was localised
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ManagementManagementMr BZ was managed for both ADEM and HSV myelitisAcyclovir 750 mg tds ivi 10/7Methylprednisolone 500mg od ivi 5/7Paracod 1g tds poPhysiotherapyHe will be followed up at the clinic in one month to review outstanding results and to assess progressAt time of discharge there was no improvement in neurological deficit
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The EndThe End
Thank YouThank You