Download
1 / 24
E N D
Is it Epilepsy? Extra Case 1 (week 3 neuro)
PCA 45 year old woman presents with new onset seizuresand altered consciousness. HxPC Julie was talking to a co-worker when she suddenly stared, turned her head to the right, began smacking her lips, and then had a generalised tonic-clonic seizure. The seizure lasted two to three minutes. Julie does not recall anything immediately prior to or during the event and was still confused 20 minutes later. Her husband and a co-worker state that she has not been physically ill recently but over the last two months has been "having a mid-life crisis". Julie has NO PMHx, PSHx, current Meds and is NKDA. Family Hx includes HTNSHx:Graphic designer, married with one daughter. Recently decided she wanted a divorce despite lack of marital conflict. Drinks one glass of wine a day
Q1 Does Julie have epilepsy? Julie has just had a complex partial seizure with secondary generalisation (since had aura or partial seizure preceded the generalized seizure) It is impossible to diagnose this episode as part of epilepsy yet since this is her first seizure. She is also at an age unlikely to develop epilepsy. Further investigation is needed!
Q2 What is your differential diagnosis? (at least three possibilities)
Q2 What is your differential diagnosis? (at least three possibilities) • TIA • Infective meningitis / encephalitis • Psychogenic seizure • Psychoactive drugs • Brain tumour • Epilepsy All acting as epileptogenic triggers If Epilepsy • Partial seizure with secondary generalisation • Primary generalized tonic – clonic seizure • Absence seizure associated with generalized tonic - clonic seizure
Q3 What signs will you look for on examination, and what laboratory tests will you order to aid in diagnosis?
Q3 What signs will you look for on examination, and what laboratory tests will you order to aid in diagnosis? O/E • Obs – (HR, BP, O2sats) – sympathetic overdrive and cyanosis during seizure episode • Temp – infection? • Lymphadenopathy • Head trauma – epileptogenic centre or consequence of seizure? • Organomegaly – storage diseases/ endocrine/ metabolic disease? • Acute psychosis? MMSE • CVS exam – risks for cerebrovascular disease • Neuro exam – signs of increased ICP – blown pupils etc, other focal neuro defects. Tests of motor func – pronator drift, tendon reflexes, gait, coordination – lesion in motor cortex? And failed double simultaneous stimulation may suggest lesion in parietal cortex. Unilateral facial droop with contralateral hemiplegia/ hemiparesis • EEG • Wet crotch? • Bitten tongue? • Any paralysis – still present after a few hours – stroke?
Q3 What signs will you look for on examination, and what laboratory tests will you order to aid in diagnosis? Investigations • U+E’s including K, Mg and Ca • Glucose • LFT’s • TFT’s • Creatinine • D - dimer • Alkaline phosphatase • Drug tox screen • LP esp in AIDS pts • MRI > CT for mass lesions, oedema, midline deviation, trauma
O/E Afebrile; BP 110/70; HR 76; RR 16 Mental State: initially responds only to simple commands and is unable to converse but over the course of your examination she improves dramatically and complains of a bifrontal headache. Julie tells you that she had a minor sore throat and possibly a low-grade temperature a week ago. She denies having any prior headaches or seizures. When asked about any changes in mood she denies this and says that she has not been depressed but feels that she needs to be free to pursue her dream of becoming a movie star. She plans on divorcing her husband and moving to Los Angeles “to be discovered”. She has no training or experience as an actress, does not plan on going to acting school and has never performed in a play since primary school. She denies any hallucinations.
O/E CN II-XII intact Fundi: no papilloedema. Visual fields NAD Motor: normal muscle tone and strength bilaterally to testing Reflexes: 2+ throughout. Babinski signs present bilaterally. Sensation, Co-ordination & Gait: NAD Investigations: Bloods NAD CT scan: poorly circumscribed, hypointense left temporal lobe lesion with small foci of haemorrhage and possible early uncal herniation, with minimal surrounding oedema.
Q4 What is the most likely diagnosis? Astrocytoma, more specifically a glioblastoma/ glioblastoma multiforme creating a mass lesion resulting in uncal herniation since these tumours can present commonly with seizures and sometimes personality, mood and mental ability changes. • Haemorrhage suggests aggressive nature (infiltration and necrosis), therefore placing provincial diagnosis on GBM (high grade IV) over diffuse astrocytoma (grade II) or anaplastic astrocytoma (grade III). If endothelial proliferation was present, this would rule in GBM • Location and behavioural Sx suggest Dx of neuronal tumour, BUT haemorrhage and Julie’s age don’t add up • Julie is abit old for embryonal tumours • Lack of calcification oligodendroglioma less likely • Location makes ependymoma and meningioma less likely too • Single lesion make metastatic brain tumour unlikely
Q5 What would be the next step in management? • Treat with anti-epileptics • Order indicated investigations : MRS, PET but NOT LP (unless you don’t like your registration – transtentorial herniation happens) • Treat the oedema: IV corticosteroids and mannitol
Julie's MRI shows a large, poorly circumscribed cortical, left temporal lobe lesion with areas of haemorrhage and necrosis. The uncal herniation is mild with no evidence of brainstem compression. A biopsy is taken.
Q6 What is the most common primary brain tumour in adults? Gliomas – High grade infiltrating astrocytoma (60 – 80 % of the little blighters) aka ‘the terminator’
Q7 Briefly outline management of this condition • Potato poultice twice daily applied to ear • 53 sessions of chiropractic realignment
Q7 Briefly outline management of this condition. Assuming GBM: • Biopsy/ Sterostatic biopsy (appropriate management can only occure once definitive histological Dx made) • Preoperative Imaging (determine the functional regions of the brain and the location of the lesion in relation to these) • Surgical Resection as appropriate (Maximal resection whilst preserving neurological function) • Adjunctive Radiotherapy • Adjunctive Chemotherapy • Temozolomide – oral alkylating agent – 1o • The nitrosurea ‘carmustine – iv alkylating agent – 2o • Nice things like pt education, support groups etc – most GBM- suffers die within a year of diagnosis, even with treatment. Less than 2% survive 3 years with the condition.
