Pseudohernia abdominal como complicación infrecuente de herpes zóster cutáneo: reporte de un caso / Abdominal pseudohernia as a complication infrequent cutaneous herpes zoster: report of a case

Una de las infecciones virales más comunes -sobretodo en personas de mayor edad- es el Herpes Zóster (HZ). Su característica clínica, hace sospechar al médico de forma temprana, para otorgar un tratamiento adecuado y oportuno. Dentro de las complicaciones más frecuentes se encuentran las sensitivas, como la neuralgia postherpética.1 Sin embargo, existen un grupo de complicaciones motoras de menor incidencia, como lo es la Pseudohernia abdominal. Ésta corresponde a una paresia segmentaria, que se manifiesta como una protrusión de la pared abdominal sin un defecto real, que aumenta con maniobras de valsalva.1 Generalmente se puede presentar en hombres, mayores de 60 años, inmunosuprimidos o con neoplasias hematológicas.1,2,3 El diagnóstico es clínico, aunque se puede confirmar con estudio imagenológico, que evidencie una musculatura de la pared abdominal adelgazada con respecto a la contralateral y que descarta un orificio herniario por un defecto estructural. 2 La electromiografía también puede jugar un rol al evidenciar anormalidades en la conducción nerviosa. 2 La pseudohernia por HZ tiene un buen pronóstico en la mayoría de los pacientes con recuperación completa: entre 2-18 meses. 3 Su principal riesgo es la pseudobstrucción intestinal, que se puede manifestar como constipación.2,4 En el siguiente reporte de caso, se analiza a la pseudohernia abdominal como complicación motora infrecuente del HZ y sus características.

One of the most common viral infections -especially in elderly- is Herpes Zoster (HZ). Its clinical characteristic makes the doctor suspect early, to grant adequate and timely treatment. Among the most frequent complications are the sensitive ones, such as postherpetic neuralgia1 . However, there is a group of motor complications of lower incidence, such as abdominal pseudohernia. This corresponds to a segmental paresis, which manifests as a protrusion of the abdominal wall without a real defect that increases with valsalva maneuvers1 . It can generally present in men, older than 60 years, immunosuppressed or with hematological neoplasms1,2,3, The diagnosis is clinical, although it can be confirmed with an imaging study, which shows a thinner abdominal wall musculature with regard to the contralateral wall, and which rules out a hernial orifice due to a structural defect2 . Electromyography can also play a role in show abnormalities in nerve conduction2 . HZ pseudohernia has a good prognosis in most patients with complete recovery: between 2-18 months.3 Its main risk is intestinal pseudoobstruction, which can manifest as constipation2,4. In the following case report, abdominal pseudohernia is analyzed as a rare motor complication of HZ and its characteristics.

Non-compressive myelopathy: clinical and radiological study.

Fifty seven patients (42 males and 15 females) with non-compressive myelopathy were studied from 1997 to 1999. Acute transverse myelitis (ATM) was the commonest (31) followed by Vit B12 deficiency myelopathy (8), primary progressive multiple sclerosis (5), hereditary spastic paraplegia (3), tropical spastic paraplegia (2), subacute necrotising myelitis (1), radiation myelitis (1), syphilitic myelitis (1) and herpes zoster myelitis (1). 4 cases remained unclassified. In the ATM group, mean age was 30.35 years, antecedent event was observed in 41.9% case, 25 cases had symmetrical involvement and most of the cases had severe deficit at onset. CSF study carried out in 23 patients of ATM revealed rise in proteins (mean 147.95mg%, range 20-1200 mg/dL) and pleocytosis (mean 20.78/cumm, range 0-200 mm3). Oligoclonal band (OCB) was present in 28% of cases of ATM. The most common abnormality detected was a multisegment hyperintense lesion on T2W images, that occupied the central area on cross section. In 6 patients hyperintense signal was eccentric in location. MRI was normal in 4 cases of ATM. Thus ATM is the leading cause of non-compressive myelopathy. Clinical features combined with MRI findings are helpful in defining the cause of ATM.