PROF DR K H NOOR UL AMEEN M6 UNIT

DR.RAKESH PINNINTI

CASE OF GIDDINESS

Chief complaints

Mr. Elumalai aged 25yr a transport vehicle driver presented with complaints of

a) Giddiness 3 months b) Headache 1 week c) Fever 1day (1week ago)

Presentation

Patient was apparently doing well 3 months back....

On the day of onset of his symptoms patient experienced intense giddiness around 2pm while he was having a conversation with his friends, within minute or two he had a complete black out & later regained consciousness, was informed of fall & unconsious state that lasted for 4-5 min.

H/O nausea preceded the event.

Presentation

Patient had similar episode 15-20days later but Patient wasn’t sure of the events that happened during the blackout period as those events always happened during his work as a driver in different towns , patient never had an accident from his symptoms, stopped driving after 3rd episode,

After each episode patient felt fatigued & unable to concentrate for the rest of the day.

Now patient only complains of giddiness, not had LOC after the 3rd episode.

Presentation

Patient has Headache since 1 week, diffuse distribution of pain, intermittent throbbing quality initially, but patient having dull ache since 2 days

No specific time / diurnal variation with pain except that sometimes pain severe early morning

Pain adequately relieved on taking analgesics

Presentation

No h/o chest pain; palpitations; dyspnea;

No h/o altered sensorium; nausea; vomiting.

No h/o memory disturbances, diplopia, dysphagia, weakness of limbs, loss of sensation, incordination, bowel;bladder disturbances.

No h/o reduced urine output/passage of stool ova/cyst; bleeding tendency/bleedingfrom any orifice.

HISTORY

Past History: No relevant past history; not a K/C/O DMT2; SHT; RHD; Seizure disorder.

Family History: Nothing significant

Personal History: not a smoker or alcoholic no bowel bladder disturbances mixed diet disturbed sleep since 3 months

Examination

Patient an young adult male aged 23 yr moderately built & nourished.

conscious, oriented, responds & obeys commands, moves all 4 limbs.

His vitals were stable, He is not anemic not jaundiced, no cyanosis, no

clubbing ,no generalized lymphadenopathy.System examination revealed no significant

cardiovascular / respiratory abnormal findings.

CNS

HIGHER MENTAL FUNCTIONS

Patient was conscious, oriented in time, place & person, MMSE >25 no cognitive impairment (short orientation

memory conc test)

normal speech & articulation

CNS

CRANIAL NERVES

Pupils : Size R 4mm; L 3mm B/L brisk reaction to light &

accommodation Fundus Normal

No other significant cranial nerve palsies observed.

MOTOR SYSTEM

R L

TONE: NORMAL NORMALBULK: NORMAL NORMALPOWER UL 5/5 5/5 LL 5/5 5/5REFLEXES biceps N N Triceps N N Ankle BRISK BRISK Knee BRISK BRISKPLANTAR FLEXOR FLEXOR`

SENSORY SYSTEM & CEREBELLAR SIGNS

NO SIGNIFICANT ABNORMALITY NOTED CLINICALLY

List of problems

Black outs ?syncope;?seizuresGiddinessHeadache Brisk reflexes on examination

A point score to identify cardiac syncope was developed in a multicenter cohort of 260 patients with syncope evaluated according to 2004 ESC guidelines

1) Palpitations preceding syncope - 4 points 2) Heart disease and/or abnormal electrocardiogram

(sinus bradycardia, second or third degree atrioventricular block, bundle branch block, acute or old myocardial infarction, supraventricular or ventricular tachycardia, left or right ventricular hypertrophy, ventricular

preexcitation, long QT, Brugada pattern) 3 points3) Syncope during effort - 3 points 4) Syncope while supine - 2 points 5) Precipitating or predisposing factors (warm-crowded place,

prolonged orthostasis, pain, emotion, fear) - minus 1 point 6) A prodrome of nausea or vomiting - minus 1 point

A score of ≥ 3 had 92 percent sensitivity and 69 percent specificity for cardiac syncope in the validation cohort.

Investigations

Imaging CT scan Brain

MRI

XRAYS

Several X rays taken so to demonstrate active/ calcified lesions

But no findings suggestive of tissue cysticercosis were found.

INV further

C.S.F CYSTICERCAL ANTIBODIES

EEG - NORMAL

ECHO - NORMAL

Muscle biopsy

Stool ova cyst larvae - NIL

B scan of Orbit

Diagnostic criteria

The presence of two different lesions highly suggestive of neurocysticercosis on neuroimaging studies should be considered as two major diagnostic criteria..

MUSCLE BIOPSY

Macroscopic: skeletal muscle tissue 1cm*.7cm with a cystic lesion observed.

Microscopy: skeletal muscle fibers noted with parts of cystic inflammatory lesion consistent with cross sectional scolex noted with peri-lesional inflamation with eosinophil infiltrate

Intra scolex features consistent with mouth parts with no evidence of hooklets

IMP: FEATURES CONSISTENT WITH CYSTECERCOSIS

DIAGNOSIS

Parenchymal Neurocysticercosis (NCC) – STAGE 1 vesicular cysts

Sub-cutaneous & Intra-muscular cysticercosis

TREATMENT

The initial approach to patients with clinical manifestations of neurocysticercosis (NCC) should focus on management of symptoms such as seizure control with antiepileptics and treatment of increased intracranial pressure, if present.

Subsequently a determination should be made regarding the role of antiparasitic and anti-inflammatory therapy.

Antiepileptic therapy

Antiepileptics should be administered to patients with NCC who present with seizures.

Most reports in the literature on management of seizure due to NCC describe use of phenytoin or carbamazepine.

Antiepileptic therapy may also be appropriate for patients who do not present with seizures but who are at high risk for seizures. The risk of seizures appears to be highest in the setting of multiple lesions.

Calcified, inactive lesions can also serve as foci for seizures but in an otherwise asymptomatic patient are not generally considered an indication for prophylactic antiepileptic drug therapy

The optimal duration of antiepileptic therapy is uncertain; most experts favor administering antiepileptic therapy for 6 to 12 months after radiographic resolution of active parasitic infection.

Antiparasitic therapy

Consensus on the optimal role of antiparasitic therapy in the setting of cysticercosis is beginning to emerge.

The potential benefit of antiparasitic therapy for treatment of neurocysticercosis is hastened resolution of active cysts, decreased risk for seizures, and decreased recurrence of hydrocephalus.

The potential risk of treatment with antiparasitic therapy is exacerbation of neurologic symptoms due to increased inflammation around the degenerating cyst, particularly in patients with a large number of lesions. The inflammation can be so severe that it can lead to disability or death

Albendazole

Albendazole (15 mg/kg per day [usually 800 mg/day in two divided doses; taken with food to increase bioavailability]) facilitates the destruction of parenchymal cysticerci.

The optimal duration of therapy depends on the form of disease.

a) Patients with a single enhancing lesion appear to benefit from a short course of therapy (3 to 7 days).

b) Patients with multiple viable parenchymal lesions should receive a longer course of treatment (10 to 14 days);

c) Patients with subarachnoid disease may benefit from prolonged therapy guided by the response on imaging studies (≥ 28 days)

Praziquantel (50 to 100 mg/kg per day in three divided doses) is an alternative to albendazole.

Anti-inflammatory therapy

Corticosteroids should be administered to patients with parenchymal neurocysticercosis receiving treatment with antiparasitic therapy, to reduce inflammation associated with the dying organisms.

Doses used are typically 1 mg/kg/d of prednisone or prednisolone or 0.1 mg/kg/d of dexamethasone for 5 to 10 days followed by a rapid taper.

Prior to the initiation of therapy with antiparasitic medications or corticosteroids, screening for latent TB infection, strongyloidiasis and ocular cysticercosis should be pursued

Multiple cysts

In the setting of multiple parenchymal cysts, active and inactive cysts may be present in the same patient simultaneously.

Administration of antiparasitic therapy may hasten degeneration of viable cysts, thereby increasing inflammation at the site of these lesions and potentially increasing risk for seizure.

Nonetheless, most favor treatment of multiple viable, parenchymal cysticerci with antiparasitic therapy (albendazole 15 mg/kg/d in two daily doses for 8 to 15 days) administered together with high-dose steroids

Cysticercal encephalitis — Cysticercal encephalitis (diffuse cerebral edema associated with multiple inflamed cysticerci) is a contraindication for antiparasitic therapy, since enhanced parasite killing can exacerbate host inflammatory response and lead to diffuse cerebral edema and potential transtentorial herniation. Most cases of cysticercal encephalitis improve with corticosteroid therapy.

STAGES OF NCC

The four stages of cysts within the parenchyma of the brain: vesicular, colloidal, nodular/granular, and calcified granulomas.

The viable larval cyst is known as a vesicular cyst and has minimal enhancement, which is due to little or no host immune response. At this stage, the scolex usually is identified as an eccentric nodule within the cyst.

As the cyst degenerates, fluid from the larval cyst leaks into the parenchyma, generating a strong immune response, characterized by enhancement on contrast computed tomography (CT) and magnetic resonance imaging (MRI). An enhancing cyst, without a well-defined scolex, is termed a colloidal cyst .

As the cyst further deteriorates, it forms a nodule, which continues to demonstrate contrast enhancement.

Finally the degenerating cyst forms a calcified granuloma, which is recognized as nonenhancing punctuate calcifications on CT

Evidence based Managment

TI - A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis.

SO - N Engl J Med 2004 Jan 15;350(3):249-58

TI - Perilesional brain oedema and seizure activity in patients with calcified neurocysticercosis: a prospective cohort and nested case-control study.

SO - Lancet Neurol. 2008 Dec;7(12):1099-105.

TI - Treatment of neurocysticercosis: current status and future research needs. SO - Neurology. 2006 Oct 10;67(7):1120-7.

TI - Current consensus guidelines for treatment of neurocysticercosis. SO - Clin Microbiol Rev 2002 Oct;15(4):747-56

TI - A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis.

SO - N Engl J Med 2004 Jan 15;350(3):249-58.

TI - Short course of prednisolone in Indian patients with solitary cysticercus granuloma and new-onset seizures.

SO - Epilepsia. 2003 Nov;44(11):1397-401.

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