Neurocysticercosis Most common parasitic infection of CNS Most common cause of acquired epilepsy in Incidence 4% in some areas. Incubation period within 7 years from exposure (83%). Spinal cord and peripheral nerve involvement is rare. Occurs from ingesting the parasite’s eggs, not from eating infested meat T. solium can infect a person in two different ways: as the adult worm or as the larva.
Commonly involved sites ● brain: involved in 60–92% of cases of cysticercosis . Latency from ingestion of eggs to symptomatic neurocysticercosis : 2–5 years ● skeletal muscle ● eye: immunologically privileged, like brain ● subcutaneous tissue ● heart
Many larvae die naturally within 5–7 yrs or with cysticidal therapy producing an inflammatory reaction with collapse of the cyst (granular nodular stage); these sometimes calcify ( nodular calcified stage).
Giant cysts Cyst with diameter > 50 mm . Two types of cysts tend to develop in the brain: 1 . cysticercus cellulosae : in the parenchyma or narrow subarachnoid spaces. It contains a scolex ( head), is usually static, and produces only mild inflammation during the active phase 2. cysticercus racemosus : larger (4–12 cm), grows actively producing grape-like clusters in the basal subarachnoid spaces & fourth ventricle and produces intense inflammation.
4 Location of the cysts Meningeal: found in 27–56% of cases with neural involvement. Parenchymal : found in 30–63%; focal or generalized seizures occurs in ≈ 50% of cases (up to 92% in some series) Ventricular: found in 12–18%, possibly gaining access via the choroid plexus. Intermittent intracranial hypertension ( Brun syndrome ). 4. Mixed lesions : found in ≈ 23%
DX Laboratory evaluation Mild peripheral eosinophilia CSF Stool : less than 33% of cases have T. solium ova in the stool. Serology Most centers use enzyme-linked immunoelectrotransfer blot (EITB) against glycoprotein antigens (western blot), which is ≈ 100% specific and 98% sensitive , although sensitivity is less (70%) in cases with a solitary cyst.
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Treatment Medical 1. Anthelmintic : antiparasitic and/or cysticidal : Praziquantel vs Albendazole vs Niclosamide NB: Needed even following surgery. 2. Antiepileptics : 3. Steroids: must precede (3 doses) anthelmintic in incresed ICP No Rx needed: HCP, calcified, high burden Surgical : A) Establish DX: stereotactic vs open biopsy B) Spinal cysts and for intraventricular cysts C) Ventricular CSF diversionary procedures D) Giant cysts when intracranial hypertension does not respond to steroids E) Mesial temporal lobe epilepsy with hippocampal sclerosis caused by NCC F) Hydrocephalus secondary to cysticercotic arachnoiditis
Echinococcosis ( hydatid cyst ) Caused by encysted larvae of the dog tapeworm Echinococcus granulosa in endemic areas. The dog is the primary definitive host of the adult worm. Intermediate hosts for the larval stage include sheep and man. Man is infected either by eating food contaminated with ova, or by direct contact with infected dogs
CNS involvement occurs in only ≈ 3 % ( less in spinal cord ) Confined to the white matter. Most commonly located supratentorially , parietal lobe commonest ; MCA territory The cyst enlarges slowly (rates of ≈1 cm per year, higher in children ) contains germinating parasitic particles called “ hydatid sand” containing ≈ 400,000 scoleces /ml Primary cysts are usually solitary vs secondary cysts Intracranial hydatidosis is rare and more affects pediatric age group . CT density of the cyst is similar to CSF .
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Treatment Surgical removal of the intact cyst: Dowling technique Avoid cysts ruptur during removal, Scoleces may contaminate the adjacent tissues with possible Recurrence of multiple cysts or Allergic reaction. Adjunctive medical treatment with albendazole for 28 days
Role of medical Rx for small or inoperable brain cysts Medical therapy has shown promising effects but surgery remains the golden treatment and results in a complete cure. Chemotherapy is indicated for inoperable patients with primary liver/lung echinococcosis and for patients with multiple cysts in two or more organs.
Amebic infections of the CNS Rare The ameba lives in fresh water and soil Naegleria fowleri : the only ameba known to cause CNS infection in humans → primary amebic meningoencephalitis (PAM): diffuse encephalitis with hemorrhagic necrosis and purulent meningitis… ICP Rapid progression More prominent in the frontal lobes.
Pathophysiology
Lab ix CSF : cloudy and often hemorrhagic, ↑ leukocytes, ↑ protein, normal or ↓ glucose, Gram stain negative (no bacteria or fungi), wet prep → motile trophozoites (may be confused with WBCs). Fatal in ≈ 95% of cases, usually within 1 week.
Diagnosis Neuroimaging studies usually show multiple ring-enhancing lesions in patients infected with Acanthamoeba spp ., E. histolytica and B. mandrillaris and diffuse edema in those infected with N. fowleri . Examination of fresh CSF may reveal mobile trophozoites in patients with N. fowleri encephalitis
Treatment Medical : 6-week course of amphotericin B, rifampicin, and chloramphenicol Surgical intervention : drainage of a brain abscess ventriculostomy with CSF
CNS toxoplasmosis Occurs late in the course of HIV infection, usually when CD4 counts are < 200 cells/mm3. Present as: 1. Mass lesion (toxoplasmosis abscess): the most common lesion-causing mass effect in AIDS patients (70–80% of cerebral mass lesions in AIDS) 2 . Meningoencephalitis 3 . Encephalopathy
CT/MRI findings in toxoplasma abscess 1 . most common findings: large area (low density on CT) with mild to moderate edema, ring enhancement with IV contrast in 68% compatible with abscess (of those that did not ring-enhance, many showed hypodense areas with less mass effect, with slight enhancement adjacent to lesion), well circumscribed margins51 2. most commonly located in basal ganglia , are also often subcortical 3. often multiple (typically > 5 lesions) and bilateral 4. usually with little to moderate mass effect (in BG, may compress third ventricle and Sylvian aqueduct , causing obstructive hydrocephalus) 5. most patients with toxoplasmosis had evidence of cerebral atrophy
Treatment Pyrimethamine + sulfadiazine + Folinic acid Clindamycin, clarithromycin, trimetrexate , piritrexim , and atovaquone are alternative drugs in patients in whom skin reactions to sulfadiazine develop
Role of surgery: settling DX A) in patient with a negative toxo titer b) accessible lesion(s) atypical for toxo (i.e., Non-enhancing, sparing basal ganglia, periventricular location) c) in the presence of extraneural infections or malignancies that may involve the CNS d) lesion that could be either lymphoma or toxo (e.g. Single lesion e) in patients who have lesions not inconsistent with toxo but fail to respond to appropriate anti- toxo medications in the recommended time F) the role of biopsy for non-enhancing lesions is less well-defined as the diagnosis does not influence therapy G) stereotactic biopsy may be especially well-suited, with up to 96% efficacy, fairly low morbidity (major risk: significant hemorrhage, ≈ 8% incidence), and low mortality
Neuroschistosomiasis ( CNS Schistosomiasis ) occur by either an ectopic worm or egg dissemination via the bloodstream through retrograde venous flow into the Batson vertebral epidural plexus.
Spinal vs cerebral schistosomiasis Schistosoma mansoni is the primary cause of spinal cord disease among all species of Schistosoma . Acute myelopathy is the most common neurological complication . Schistosoma japonicum appears to cause more clinical cerebral involvement than S. mansoni . Symptomatic acute cerebral schistosomiasis due to S. japonicum has been recorded in approximately 2—4% of patients. Neurological complications can occur during all phases of schistosomiasis
Pseudotumoral encephalic schistosomiasis (PES) The tumor-like mass can be located in any region of the brain, but the cerebellum is the most common site , followed by the occipital and frontal lobes.
DX Biopsy of the nervous tissue is the only method that gives a definite diagnosis of SCS However , this procedure should be avoided because of its risks. The diagnosis of SCS has been established according to the following criteria: Evidence of lower thoracic or upper lumbar neurological lesions; Detection of exposure to schistosomiasis through parasitological or serological techniques; and Exclusion of other causes of myelitis.
Treatment Schistosomicidal drugs, steroids and surgery are currently the available treatments for neuroschistosomiasis . Praziquantel is the treatment of choice for all schistosome species.
Indication for Surgery VPS for hydrocephalus and intracranial hypertension in cerebellar schistosomiasis . Surgical intervention such as decompressive laminectomy when acute s. Mansoni myelitis deteriorates despite clinical treatment. Refractory epilepsy
References Greenburg 9 th ed Youm a n 7 th ed Schimedik & Sweet 6 th ed CDC Up-to-date Journals