Today we talked about the case of a young woman who presented after suicide attempt by ingestion of multiple prescription medications, found to be obtunded, initially in status epilepticus and later with exam findings concerning for serotonin syndrome.
- Continuous EEG is indicated if a patient is not returning to baseline mentation 15 mins after a seizure to rule out non-convulsive status epilepticus.
- Status epilepticus is defined as a seizure lasting > 5 mins or > 2 discrete seizures between which there is incomplete recovery of consciousness.
- Treatment of status epilepticus involves acute management with IV/IM benzos, urgent long-term control with IV fosphenytoin (preferred), phenytoin, or valproic acid. Remember that keppra is more useful in suppressing future seizures than treating an acute episode.
- Serotonin syndrome is a clinical diagnosis and manifests with neuromuscular activation like tremors, hyperreflexia, and clonus (generally worse in lower extremities). Use Hunter’s criteria to help with diagnosis.
- When is continuous EEG needed?
- If patient is not returning toward baseline in 15 mins after a seizure, goal is to rule out nonconvulsive seizures
- How to define status?
- > 5 mins OR
- > 2 discrete seizures between which there is incomplete recovery of consciousness
- Non-convulsive status epilepticus
- Suspect if LOC not improving by 10 mins after cessation of movement
- Mental status remains abnormal for 30-60 mins after movement cessation
- Dx requires a 24-hour EEG (we don’t have one ☹)
- Treatment is the same as generalized status epilepticus, but prognosis is worse (mortality 65% vs 27%)
- Treatment of status
- Assessment and supportive treatment
- Initial pharmacologic therapy
- Ativan (2 mg IV q1-2 mins), total dose 0.1mg/kg
- Watch out for respiratory depression and hypotension
- Alternatives: versed 0.2mg/kg IM, valium 0.2mg/kg IV
- Urgent long-term control
- Fosphenytoin (preferred): 20 mg/kg at 150mg/min
- Give extra 10 mg/kg if not responding
- Dephosphorylates into phenytoin. It’s more soluble in water and less likely to precipitate in the skin and vessels.
- Phenytoin: 20mg/kg at 50mg/min (slower than fospheny)
- If infused too fast, can irritate skin/vessels causing skin necrosis
- Valproic acid: 20mg/kg at 5 mg/kg/min
- Sometimes the preferred choice in patients with known generalized epilepsy b/c phenytoin can provoke absence seizures in that population.
- What about Keppra?
- Technically not FDA approved for status. It has weak evidence to support its use. More useful in suppressing subsequent seizures after status has been controlled.
- Clinical diagnosis. Serum serotonin concentrations do not correlate with clinical findings.
- Severe disease can lead to DIC, rhabdo, renal failure, and ARDS.
- Diagnostic criteria: use Hunter’s (84% sensitive, 97% specific)
- Anticholinergic toxicity
- Malignant hyperthermia
- Sympathomimetic intoxication
- Sedative-hypnotic withdrawal
- Serotonin syndrome may be distinguished from other causes of agitated delirium on the basis of neuromuscular findings. Whereas patients with serotonin syndrome show signs of neuromuscular activation (eg, tremor, hyperreflexia and clonus that are greater in the lower extremities, ocular clonus, and increased muscle tone), patients with sympathomimetic toxicity or infections of the central nervous system lack these findings.
- Supportive care and sedation
- Chemical sedation preferred over physical restraint
- Autonomic instability
- High BP: esmolol or nitroprusside (Short acting). Avoid longer acting agents
- Low BP: neo or epi. Avoid idirect agents like dopamine because they are converted to epi and norepi. When monoamine oxidase is inhibited, epi and norepi production at the cellular level is not controlled and could lead to an exaggerated HD response.
- No benefit to Tylenol b/c increase in body temp is due to increased muscular activity rather than alteration in the hypothalamic temperature setpoint.
- If temp >41.1, then sedate, paralyze, intubate
- Antidote: cyproheptadine
- Histamine receptor antagonist. Also has weak anticholinergic activity
- 12 mg loading dose, then 2 mg q2h until clinical response is seen.
- Is sedating (good) and can also cause transient hypotension.
We have a very bizarre case of a 23 year old woman, with a history of hypertension, presenting as a stroke alert. She has dysarthria and focal right-sided deficits, and she required intubation for airway protection. She has no prior stroke or clotting history, no illicit drug use (other than marijuana), and no significant family history. CT of the head was unremarkable, but CTA revealed a… vertebral artery dissection! We later learned that the patient was in the middle of getting a massage when the stroke occurred!
That’s right, this is a case of cervical artery (more specifically the vertebral artery) dissection secondary to traumatic massage!
Stroke typically is due to atherosclerotic disease in most cases, but if you need a case that occurred in a young patient, and you’ve ruled out everything else that would present similar, consider the following:
Stroke in young patients
- APLS (one of the most common)
- Hypercoagulable/hyperviscosity states
- Primary: Takayasu, GCS, Kawasaki, PAN, ANCA
- Secondary: TB, HIV, syphilis, fungi, SLE
- Dissection (most common in young patients)
- Structural malformation i.e. AVM, aneurysms
- Cerebral venous sinus thrombosis
- Fabry’s disease
- Congenital defects
- PFO/ASD leading to paraoxysmal stroke
- Rheumatic valve disease
Vertebral artery dissection:
- Can occur at any age and usually infrequent, but vertebral arterial dissection in general is a common cause of stroke in the young.
- Carotid artery dissection is much more common than vertebral.
- Incidence: 1-1.5 per 100,000.
- Spontaneous dissections of the carotid and vertebral artery account for ~ 2% of ischemia strokes but in young and middle age patients, they can account up to 10-25%.
- Peak incidence at 5th decade of life, occurs earlier in F > M
- Most of these patients likely have underlying connective tissue pathology leading to weakening of artery structural integrity but this is a theory.
- False lumen expansion leading to cerebral ischemia from hypoperfusion or thromboembolism, also can cause neurological sx from compression of adjacent nerves/vessels leading to CN involvement, Horner syndrome, pain, etc.
- Main mechanism, as revealed by angiography studies, point toward a thromboembolic mechanism from the dissection leading to stroke.
- Hemorrhage due to rupture, expanding hematoma can also lead to focal neurological signs.
- Connective tissue disorders (i.e. Ehlers Danlos, Marfans, ADPKD, osteogenesis imperfecta, subclinical/unnamed)
- Painting a ceiling
- Sudden neck movement
- Chiropractic manipulation, estimated 1 in 20000 spinal manipulations lead to a stroke.
- Most cases have a precipitating event
- Intracranial dissection
- 50% of cases result in subarachnoid hemorrhage
- Extracranial dissection
- Associated with trauma, vertebral artery is most mobile and vulnerable to mechanical injury at C1 to C2 as it leaves the transverse foramen of the axis vertebra and enters the intracranial space.
- Severe neck pain, dizziness, vertigo, double vision, ataxis, dysarthria are common symptoms.
- Lateral medullary and cerebellar infarctions are common
- Typical: Local pain, HA, ipsilateral Horners, CN palsies, hemiparesis typically ipsilateral
- Exam: Hematoma, vascular bruit (1/3 in carotid dissections, usually absent on vertebral), Horner’s syndrome, neck tenderness
- Catheter angiography used to be the gold standard, nowadays moving toward…
- Anticoagulation for at least 3-6 months to prevent thromboembolic complications unless there is hemorrhagic transformation of the infarct, an intracranial aneurysm, or intracranial extension.
- Most ischemic damage is actually due to thromboembolic effect, not hypoperfusion.
- Surgical: May be required for SAH/intracranial VAD or if the defect fails to heal on its own
- Endovascular stenting used for extracranial carotid or vertebral artery dissection when medical mgx fails, anticoag or thromboiysis does not exclude subsequent endovascular therapy but ideally endovascular intervention should be done within 6 hours.
- Thrombolytics: Consider in extracranial dissection, contraindicated in intracranial dissections or aorta involvement.
- Extracranial VAD: Generally has good prognosis, estimated 50% of patients will recover with no neurological deficit and 25% with moderate to severe deficits.
- Intracranial VAD: Prognosis is generally pretty poor.
Take Home Points:
- Cervical (Carotid more common than vertebral) artery dissection is a common cause of strokes among young patients.
- Chiropractic manipulation, even massages, are risk factors for cervical artery dissection!
- A good portion of patients with cervical artery dissection might have underlying, sometimes subclinical, connective tissue abnormalities.
We presented a case of a 63yo M with 30-pk-yr tobacco use, HTN, HLD, and prior CVD 7 months ago presenting with acute onset vision loss of the left eye, described as “seeing through a black mesh with spots of clear vision.” His symptom lasted for 2 hours before gradually resolving on its own. His cardiovascular and neuro exam were unremarkable, and his fundoscopic exam was normal other some mild AV nicking (a sign found with long standing hypertension). Labs and imaging including CTA did not find any acute etiology. A MR of the orbit was also done without any abnormal findings.
Ultimately pt was diagnosed with transient monocular vision loss (TMVL) most likely secondary to an episode of TIA!
Common things being more common, the most common cause of transient monocular vision loss is ischemia/vascular related!
- CRVO: Classic painFUL vision loss, flame hemorrhage (blood and thunder descriptor) on fundoscopic exam
- Acute angle closure glaucoma is the most common factor predisposing to retinal retinal vein occlusion
- Other risk factors: Sickle cell, HIV, Waldenstrom, sarcoidosis, syphilis
- CRAO: Classic painLESS vision loss, cherry red spot with retinal pallor is a classic description
- Carotid artery syndrome (transient retinal hypoperfusion or microemboli)
- Optic neuritis
- Optic nerve ischemia
- Increased ICP
- Association with polymyalgia rheumatica
- Typical patient demographics: Age > 55, F > M (2:1), Scandinavian/Northern European ancestry
- Other associated sx: Fever, headache, jaw claudication, scalp tenderness
- ESR and CRP typically elevated but this is NOT always the case!
- Smart phone use in the dark (I am not kidding), please see this article for more details
Management of TIA
In addition to treating risk factors i.e. HTN, HLD, DM2, a question often came up…
To DAPT or not DAPT?
CHANCE, a multicenter, randomized, placebo-controlled trial published in 2013 (Wang et al.) in the NEJM, revealed that DAPT within 24 hours after a TIA or mild ischemic stroke is beneficial in reducing 90-day stroke risk without an increase in bleeding complications vs aspirin monotherapy. This study was done in China with a patient population with higher incidence of undertreated modifiable risk factors and greater cerebral vascular disease burden, hence its applicability to an American patient population is unclear.
Then the POINT trial came along funded by the NIH, which saw the same benefit in DAPT after TIA/ischemic stroke but with increased bleeding risk compared to aspirin monotherapy.
Bottomline: CHANCE indicates 21 days of DAPT post TIA/ischemic stroke is helpful without increasing bleeding risk, and in POINT, 90 days of DPT is also beneficial but it increases bleeding risk. Per 2018 AHA/ASA guideline:
- In patients presenting with minor stroke, treatment for 21 days with dual antiplatelet therapy (aspirin and clopidogrel) begun within 24 hours can be beneficial for early secondary stroke prevention for a period of up to 90 days from symptom onset.
Thank you Julie for presenting a case of a 27yo F with a history of Guillain Barre syndrome 2 years ago, requiring 1 year of rehab but now with full neurological recovery, presenting with numbness and tingling of her lower extremities and her hands. Her symptoms are described as “ants crawling” on her skin, which started at her feet but became progressively more superior. Also endorses involvement of her hands as well later on. She has no recent illnesses and she has no illicit drug use. Her first episode of GBS started out very similarly, hence she was concerned.
EMG revealed a primarily demyelinating polyneuropathy affecting motor > sensory nerves predominantly in the lower extremities… but wait, does it even fit her symptoms, which are primarily sensory (although mild subjective weakness)???
We will use this case to illustrate that there is a spectrum of Guillain Barre!
- All age groups affected but risk increases with more advanced age
- M > F slightly
- Most commonly associated with after an episode of campylobacter jejuni infection.
- Other culprits: VMC, EBV, HIV, Zika virus, Mycoplasma.
- Rare cases of GBS can happen after a triggering event, i.e. immunization, surgery, BMT.
- Immune response to a preceding infection that cross-reacts with peripheral nerve leading to demyelination (a form of molecular mimicry)
- Note that there are two forms of peripheral neuropathy:
- Pathophys: Disruption of the axon itself, typically presents with motor >>> sensory deficits.
- DDx: HIV, amyloidosis, B12 deficiency, Lyme disease, hypothyroidism, critical illness polyneuropathy, variant of GBS
- Pathophys: Disruption of the myelin sheath, slowing nerve conduction velocity. Both sensory and motor deficits would be present.
- DDx: GBS (classic), hereditary, infectious, drugs, certain monoclonal gammopathies.
Variants of GBS include but are not limited to…
- AIDP (Acute Inflammatory Demyelinating Polyradiculoneuropathy)
- Most common form, (85-90%)
- Disease activity usually nadirs by 4 weeks
- Progressive ascending symmetric weakness due to inflammatory demyelination
- 2-5% may develop CIDP
- CIDP (Chronic Inflammatory Demyelinating Polyradiculoneuropathy)
- Disease progression or relapses lasting longer than 8 weeks
- Most of the time does not have an antecedent/preceding event.
- Miller Fisher Variant
- 10-20% of cases
- Typical presentation: ophthalmoplegia, ataxia, areflexia.
- 25% will develop some extremity weakness
- 85-90% of pts with MFS will have GB1b antibodies positivity, strongly associated with involvement of oculomotor nerves.
- If presence of encephalitis: Bickerstaff encephalitis, possibility a spectrum of anti-GQ1b antibody syndrome.
- Acute motor axonal neuropathy (AMAN): Axonal form of GBS
- More rapid progression motor wise but sensory and DTR usually preserved.
- Most cases preceded by campylobacter infection as well
- Frequent in Asia and esp in Hong Kong, more prevalent in the summer
- More severe form is AMSAN (Acute motor and sensory axonal neuropathy)
- Pharyngeal-cervical-brachial variant
- “Localized” version of GBS
- Pure Sensory GBS
- Primarily sensory deficits with mild motor deficits.
- Timing: Progresses over 2 weeks, most cases start improving by 4 weeks. IF post-infection, sx can develop after days to weeks.
- Progressive symmetric ascending muscle weakness starting in the lower extremities and then spread upward.
- 10% of the time, muscle weakness starts in arms or facial muscles.
- Absent to depressed DTR seen in all cases
- Respiratory muscle weakness requiring ventilator support in 10-30% of cases
- 80% of patients will experience paresthesias of the hands and feet accompanying motor weakness.
- Neuropathic pain.
- Dysautonomia in 70% of cases (tachycardia, HTN/Hypotension, bradycardia, ileus, urinary retention, arrhythmias, can also see SIADH.
- CSF: LP recommended to support dx
- Elevated protein (45-200 typically but can be as high as >1000 mg/dL) with nrl WBC (albuminocytologic dissociation), seen in 50-66% in the 1st week after onset of sx, >75% of pts in the 3rd
- CSF cell count typically nrl, < 5 cells/mm3, in a minority of cases can expect to see mild elevation.
- EMG: Valuable for confirming dx but can be nrl early on the disease course.
- GQ1b antibody: associated with Miller Fisher variant
- MRI: Spinal MRI may reveal enhancement of spinal nerve roots and cauda aquina.
- Secure airway!
- Predictors of respiratory failure: inability to cough, stand, lift the head, lift the elbows, and liver enzyme elevation.
- Avoid succinylcholine in intubation, increased risk of hyperkalemia.
- Supportive care, DVT prophylaxis, bladder/bowel care, PT/OT, pain control
- Plasma exchange/IVIG is indicated in most cases, speed up recovery.
- Plasma exchange usually more effective when started within 7 days of sx onset. 4-6 tx over 8 days.
- IVIG: 0.4g/kg per day x 5 days.
- IVIG and plasma exchange also recommended for ambulatory patients who are still not seeing improvement of sx after 5 weeks.
- No role of steroids!
- Full motor recovery around 60% at 1 year. Recovery can take several years.
- 2-5% develop CIDP
- 3-7% mortality rate, 20% of patients who become ventilator dependent die of complications.
Thanks to Amran for presenting an interesting case of a 84yo M with RA on MTX & Prednisone, and an unspecified self-resolving total body rash 1 month prior to presentation, presenting with pain, redness, and vision in both eyes. Detailed fundoscopic exam was consistent with bilateral anterior granulomatous uveitis as well as retinitis, consistent with a panuveitis picture. Initial work up revealed RPR and EIA positivity, his HLA-B27 also returned positive but he has no other findings suggestive of spondylosing arthropathy. His vitreal centesis returned positive for VZV!
- Tertiary syphilis without CNS/ocular involvement
- Panuveitis secondary to VZV
- Incidental HLA-B27 without e/o ankylosing spondylitis
Let’s start off with a basic review of the eye anatomy:
The Uvea consists of the iris, ciliary body, and the choroid. Uveitis is inflammation of any of these structures.
The Standardization of Uveitis Nomenclature (SUN) Working group guidance on uveitis terminology categorizes uveitis anatomically as follows;
- Anterior uveitis; localized primarily to the anterior segment of the eye, involving iris and pars plicata.
- Intermediate uveitis; localized to the vitreous cavity and pars plana, presence of WBC in the vitreous.
- Posterior uveitis; localized to the choroid and retina.
- Panuveitis; inflammation involving anterior, intermediate and posterior uveal structure
Uveitis can be further classified into granulomatous (presence of macrophages, multinucleated giant cells) vs non-granulomatous. A granulomatous uveitis is typically more likely to be an infectious process (although can still be idiopathic or Sarcoidosis).
Etiology of Uveitis
- Usually unilateral, might have other clues such as presence of vesicles.
- Ocular toxoplasmosis for some reasons occurs more frequently in immunocompetent hosts.
- Lyme Disease
- Accounts for less than 1% of cases of uveitis but can affect any part of the eye.
- TB (Yes ocular TB exists!)
- Uncommon in North America, suspect in endemic regions and worsening sx with glucocorticoids.
- Almost exclusively in immunocompromised hosts i.e. AIDS patients.
- CD4 < 50 typically.
- Bartonella (ocular bartonellosis) aka Cat Scratch Disease:
- Typically unilateral, has a characteristic “macular star” on fundoscopic exam.
- West Nile virus
- Ebola (case reports)
- Zika virus
- Varicella Zoster Virus: Can affect any part of the eye
- Non-infectious: Most common = HLA-B27 related arthropathies and reactive arthritis, tends to be unilateral and causes an anterior uveitis picture
- Ankylosing spondylitis
- Relapsing polychrondritis:
- Juvenile idiopathic arthritis
- Psoriatic arthritis
- Reactive arthritis
- TINU (tubulointerstitial nephritis and uveitis) syndrome
- Uncommon, occurs in adolescent/young F, fever, myalgias, anemia, LFT elevation, chronic uveitis, interstitial nephritis.
- MS: Optic neuritis
- Japanese and Hispanics, bilateral panuveitis, neurological/auditory sx
- Penetrating trauma
- Rifbutin, fluoroquinolone, monoclonal ab
- Other conditions that might mimic uveitis
- Retinal tears
- Ocular melanoma
- Pigmentary dispersion syndrome
- Retinitis pigmentosa
- Treat underlying cause
- If viral: Anti-virals (acyclovir, valacyclovir), add on topical corticosteroids.
- Non-infectious uveitis: Management typically with topical steroids. If posterior, some have suggested using difluprednate or periocular glucocorticoid injections. Systemic tx is reserve for pts with bilateral disease, inability to tolerate intraocular injections, or systemic conditions i.e. Behcets.
- If refractory to steroids in non-infectious causes, can consider MTX, azathioprine, mycophenolate, cyclosporine, or tacrolimus.
- TNF alpha inhibitors u.e. adalimumab has good evidence in the tx of non-infectious intermediate, posterior, and panuveitis. Can also be considered first line in management of Behcet.
- Sulfasalazine has been shown in a few small studies to prevent HLA-B27 associated uveitis.
Please refer to this previous blog post for more details on tertiary syphilis!
Thanks to Amran for presenting the case of an elderly woman with history of “transverse myelitis” 10 years ago who presented with b/l leg weakness, numbness, and tingling, found to have several spinal cord enhancements as well as optic chiasm enhacement on T2 FLAIR imaging concerning for MS vs NMO!
- MS and NMO most commonly affect women (2:1 and 10:1 respectively).
- To meet diagnostic criteria for MS, patients must demonstrate CNS lesions in both space and time via clinical or MRI findings.
- NMP affects the optic nerve and spinal cord much more so than the brain/brainstem.
- Presence of AQP4 serum antibodies are specific to NMO.
- Treatment for acute MS flare or NMO flare involves high dose steroids or plasma exchange.
- The most effective chronic treatment for relapsing/remitting MS is natalizumab, not effective for NMO and may even be harmful.
Framework for myelopathies:
Demyelinating diseases that present with myelitis:
- Most commonly affects young adults
- Mean age of onset 28-31. Though can present between 15-50
- Affects women 2:1
- Life expectance is reduced by ~10 years
- Most common symptoms
- Sensory disturbances (90%)
- Numbness, tingling, pins and needles
- Lhermitte sign (flexion of the neck causes sensation of electric shock that radiates down the spine into the limbs). Can be seen in tumors, cervical disk herniation, and trauma as well.
- Fatigue and/or sleep disturbance (85%)
- Unrelated to amount of activity performed
- Worsened by depression
- Motor issues and spasticity (80%)
- Lower extremities most commonly affected
- Paraparesis, paraplegia
- Cognitive impairment (70%)
- Attention, executive function, short term memory
- Depression (60%) likely contributes
- Bowel or bladder dysfunction (50-75%)
- Visual disturbance (25%)
- Internuclear ophthalmoplegia
- Lost adduction and horizontal nystagmus of the abducting eye
- Lesion in the medial longitudinal fasciculus of the brainstem on the side of diminished adduction
- Convergence is preserved
- Optic neuritis
- Unilateral eye pain accentuated by ocular movement
- Variable degree of visual loss (90% regain normal vision)
- Characteristic features
- Different types
- Clinically isolated syndrome (first attack)
- Secondary progressive
- Primary progressive
- Progressive relapsing
- Heat sensitivity AKA “Uhthoff phenomenon” (80%)
- Due to slowing of neuronal conduction with increased body temperature
- McDonald Criteria (revised in 2017)
- Clinical or radiographic
- CSF studies are not indicated unless atypical presentation
- Acute episode
- Solumedrol 1 g IV x 3-5 days
- Plasma exchange
- If failed glucocortidoids
- Disease modifying therapy
- Good for relapsing-remitting MS
Sorry for posting this late!
A 38yo M with history of asthma, but otherwise healthy, presents acute onset seizure as well as LLE, LUE weakness and paresthesia. He has never had seizures before prior to this. History revealed that patient was born in Honduras, and he grew up on a pig farm, and his brother actually had a history of Taeniasis. MRI revealed a cystic structure with a thin septae/soft tissue component within, consistent with neurocysticercosis!
Let’s talk about seizures for a little bit.
In developeED countries, the most common cause of epileptic seizure is often idiopathic.
In developING countries, the most common cause of epileptic seizure in both kids and adults, is neurocysticercosis (NCC).
Neurocysticercosis: When larvae form of the Taenia solium (aka the tapeworm) move to non-GI tissues and into CNS.
Presentation: Viable (asx, many years) -> degenerating (loses ability to evade immune system, localized inflammation) -> non-viable (calcified granulomas, can still cause szx)
- Most common form of neurocysticercosis, > 60% of cases
- 3-5 years after infection but can occur > 30 years after initial exposure.
- Seizure = most common manifestation. Occur in setting of cysts degeneration or granulomas.
- Endemic areas: NCC is the most common cause of adult onset seizure
- Headaches, usually mild
- Rare complications: vision, focal neuro, meningitis, encephalitis (higher parasitic load)
- Most, however, are asx and diagnosed incidentally.
- When NCC occurs in the spine, eyes, ventricles, subarachnoid space. More commonly in adults.
- Can cause increased ICH, hydrocephalous
- Sub-arachnoid form is most severe, esp in the basilar cisterns. 5% of cases.
- Spinal: 1% of cases, can cause localized/dermatomal pain.
- Ocular: 1-3% of cases, impaired vision, eye pain, diplopia, chlorioretinitis, retinal detachment.
- Extra Neural
- Most common: muscles, subcutaneous
- Cardiac has been described…
- Stool O&P can help
- Eosinophilia is uncommon
- Imaging: Clinical history, endemic history, enhancing cystic lesion on MRI is very likely.
- CT: Useful for IDing calcifications, parenchymal cysticerci, and eye involvement
- MRI: Useful for small lesions, degenerative changes, edema, and visualizing scolices within calcified lesion
(Mahale et al. Extraparenchymal (Racemose) Neurocysticercosis and Its Multitude Manifestations: A Comprehensive Review. J Clin Neurol. 2015 Jul;11(3):203-211)
- Serology: Should be performed for confirmation Enzyme Linked Immunoelectrotransfer Blot Ab is highly sensitive and specific, but takes time and availability is limited.
- Latest IDSA Recommendation in 2018
- Calcified lesions: symptomatic management only with anti-epileptics
- Enhancing lesions
- Patients who acquired NCC in a non-endemic area should have their household members screened.
- Screen for latent TB, strongyloides infection given possibility of prolonged steroid use
- Fundoscopic exam is recommended for all patients with NCC
- Prior to anti-parasitic therapy, all patients should be treated with corticosteroids prior to initiation.
- Anti-epileptics should be used in all patients with seizures.
- Albendazole + praziquantel is better than monotherapy with albendazole if greater than 2 lesions. 1-2 lesions, monotherapy with albendazole should suffice.
- Intraventricular neurocysticercosis
- Minimally invasive surgical removal prior to antiparasitic therapy to minimize inflammatory response.
- Subarachnoid neurocysticercosis in the basilar cisterns or Sylvian fissures
- Prolong course of anti-parasitic until radiologic resolution, can last more than a year.
- Corticosteroids recommended while on treatment but methotrexate can be considered a steroid-sparing agent in patients requiring prolonged anti-inflammatory.
- Surgery case by case
- Spinal neurocysticercosis
- Combination surgery and anti-parasitics, start steroids first with evidence of spinal cord dysfunction and prior to antiparasitics
- Surgery preferred over medical management.