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Chronic and subacute meningitis diagnosis is challenging in daily neurological practice. The results we report contribute information from Latin America regarding etiologies of CSM, which can be identified after a comprehensive evaluation in a majority of cases.

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A 72-year-old man, presented with a one-week history of confusion and an anterograde amnesic disorder accompanied by confabulation, with lack of insight to his symptoms. Medical history included alcohol abuse and admitted twenty-years of alcohol ingestion (approximately 186 gr/day). Neurologic examination was notable for slightly decreased consciousness, disorientation to time, severe anterograde amnesia and unsteadiness of stance and gait with four limb ataxia. A metabolic blood panel including liver profile showed alanine aminotransferase mildly elevated (66 UI/L) with elevated gamma-glutamyl-transpeptidase (gGT: 426 UI/L). Tests for HIV, syphilis and vitamin B12 levels were negative. Review of initial brain MRI showed a symmetrical, increased fluid-attenuated inversion recovery (FLAIR) signal lesion extending through the hypothalamus, periaqueductal area, mamillary bodies, bilateral anterior thalami, chiasm, both optic tracts and posterior limbs of both internal capsules with restricted diffusion and patchy contrast enhancement (figure 1  1a-1b). A possible Wernicke-Korsakoff syndrome diagnosis was achived. Following the initial examination, the patient was initiated on prophylactic parenteral thiamine reposition. CSF analysis showed elevated proteins (174 mg/dl) and lactate concentration (2.9 mmol/L). Cytologic and immunocytochemical study showed no neoplastic processes. Screening of autoimmune antibodies in CSF and paraneoplastic antibodies in serum were negative. EEG and full-body CT scans were unremarkable. Thiamine serum levels were normal (16,5 ug/L) (blood sample collected previous to reposition).  Finally, a neurocognitive test indicated malperformance in tasks related to immediate and delayed recall and disturbances in recent and remote memory with confabulation. A new brain MRI after supplementation showed regression of the previous lesion (figure 1  2a-2b). He was discharged one month later with residual anterograde amnesia and gait instability that are still present eleven months later, at the last follow up.   Figure 1: (1) Axial FLAIR MRI sequence showing extensive, symmetrical, hyperintense lesion in chiasm and both optic tracts (1.a) and periaqueductal area, hypothalamus and posterior limb of internal capsules (1.b). (2) Axial FLAIR MRI sequence showing regression of the hyperintense lesion one month after thiamine reposition in chiasm and both optic tracts (2.a) and periaqueductal area, hypothalamus and posterior limb of internal capsules (2.b)   Wernicke’s encephalopathy (WE) prototypical clinical triad consists of motor problems such as ataxia or gait incoordination, ocular signs (commonly ophthalmoparesis and nystagmus) and mental status changes1-3. Thiamine (vitamin B1) deficiency secondary to alcoholism is the most common etiologic factor3. If left untreated or undertreated, there is an increased risk of developing a chronic sequelae: the Korsakoff’s syndrome (KS), characterized with loss of working memory and confabulation with sparing of remote memories2-4. Both syndromes together are termed Wernicke-Korsakoff syndrome (WKS). Even though diagnosis of WKS remains primarily clinical3, brain MRI findings in previously reported typical locations1-3are highly specific of this syndrome, suggesting MRI is a valuable confirmation tool. Normal thiamine serum levels shouldn’t dismiss the initial suspicion, as its blood concentration does not necessarily reflect brain tissue’s concentration4. Our case suggests that, even when MRI lesions are not characteristic, intravenous thiamine reposition should be immediately initiated if WKS is suspected, considering the patient's outcome depends on prompt diagnosis and adequate treatment.

A 30 year old male with no relevant previous medical history, consulted in the Emergency Room with a 1-month history of a sleep disorder with daily somnolence, adding 3 days before consultation temporal and spatial disorientation. Family members also referred hyperphagia. The patient didn’t present headache, fever, behavioral manifestations, or any other systemic or neurological signs or symptoms. He denied recent trips or vaccination.  Neurological examination was normal.  A contrast enhanced brain MRI was performed, revealing in T2/FLAIR weighted images a diffuse hyperintense hypothalamic and interpeduncular lesion with homogeneous contrast enhancement. General laboratory tests were normal, with negative HIV and VDRL results and normal B12 and thyroid function values. A lumbar puncture was performed, showing mononuclear pleocytosis and high protein levels, with a negative citologic test. Full body CT scan showed no alterations, and testicular ecography revealed  hypoechoic lesions and macrocalcifications suggestive of testicular cancer.  Testicular exeresis was performed, with anatomy pathology findings of seminoma. Paraneoplastic and autoimmune antibodies in CSF showed positive results for anti-Ma2 antibodies.  It was concluded that the patient had an Anti-Ma2-associated encephalitis.  Chemotherapy was started and the patient received five pulses of methylprednisolone 1g, maintaining long term treatment with high doses of prednisone. The patient had subtle clinical improvement.  3  months later, the patient consulted in the emergency room for anterograde amnesia. A new brain MRI was done, showing improvement of the hypothalamic lesion but with bilateral hippocampal hyperintensity without contrast enhancement. It was interpreted that the patient had now added an anti-Ma2-associated limbic encephalitis. A new full body CT scan was done, showing new retroperitoneal adenopathies despite chemotherapy. The patient received immunoglobulin 2g/kg and started a new oncologic treatment, with modest clinical improvement in the following months.   A new brain MRI was performed a year later, showing only slight hyperintensity in the right wall of the third ventricle in T2/FLAIR sequences and no contrast enhancement. Anti-Ma2 antibodies are usually present in men with testicular tumours, and they may be accompanied by a paraneoplastic syndrome including limbic, diencephalic or brainstem encephalitis. Brain MRI shows hyperintensity in the midbrain, diencephalon (thalamus/hypothalamus) or temporal lobes in T2/FLAIR weighted images, with almost half of these lesions presenting with contrast enhancement. CSF regularly has inflammatory changes.  Clinical presentation usually varies according to the region affected, and these patients tend to  have a good response to oncologic and immunologic treatment, with stabilization or even clinical improvement .  Even though this is a rare entity, it is important to consider it as a differential diagnosis in cases of young men with  midbrain or diencephalic lesions, since its early diagnosis and treatment could hinder its progression.

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.

A 47-year-old man with a history of aphasic seizures presented to the emergency room with a 12-hour global aphasia. Upon admission, brain MRI did not reveal acute lesions, and EEG showed sharp waves in the left frontal-temporal region. An Aphasic Status Epilepticus was diagnosed and antiepileptic treatment was initiated with adequate response. A week after the episode, a new brain MRI showed a high-signal ovoid lesion on T2-weighted and FLAIR sequences in the central part of the splenium of the corpus callosum. On diffusion-weighted images (DWI) the lesion was hyperintense with decreased apparent diffusion coefficient (ADC) values, indicating restricted diffusion consistent with a cytotoxic lesion of the corpus callosum (CLOCC). Follow-up MRI one month later showed complete image resolution. CLOCCs are secondary lesions associated with various entities in which high levels of cytokines and extracellular glutamate cause intracellular edema and reduced diffusion, a condition called cytotoxic edema, which affects vulnerable brain regions such as the splenium of the corpus callosum. In epileptic patients, CLOCCs may be due to the effect of seizures, especially prolonged ones, as well as antiepileptic treatment itself. CLOCCs are rare radiological findings and must be recognized to avoid misdiagnosis.