The exact mechanism of abdominal muscle paresis following herpes zoster is poorly understood. The spread of active inflammation from the dorsal root ganglion to the anterior horn cells and involvement of the motor nerve are assumed to be involved [11,22]. Ganglionic lesions combined of the related sensory and motor roots and severe neuritis on pathological examination findings which can easily explain the clinical  and electrophysiological signs [23]. The reason for this extremely rare complication is felt to be the dual innervations of musculature of abdominal wall. Symptoms of segmental muscle paresis usually appear within 2 to 6 weeks after the beginning of herpes zoster, and the involved myotomes correspond to the involved dermatomes. 

Diagnosis is usually suspected byclinical evidence of HZ associated with abdominal wall or flank bulging. Physical examination shows reduced or absent reflexes. To confirm the diagnosis conduction study must be done.MRI with gadoliniumto define the extent of the inflammation,exclude local entrapment of spinal nervewhich is known to be a precipitating factors for HZ [4]. Neurophysiological examination, including EMG and DSEPs, confirms motor and sensory loss in this unusual post-herpetic complication [24].

Our case presented with pseudo-abdominal hernia along with colonic constipation. Colonic pseudo-obstruction can start before, after or even simultaneously with skin eruptions.The Enteric Nervous System   may get involved due to Varicella-Zoster Virus (VZV) reactivation which is a lethal process and results in different gastrointestinal tract disorders, such as idiopathic gastroparesis, chronic intestinal idiopathic pseudo-obstruction, and acute colonic pseudo-obstruction [25]. Pathogenesis is not clear. Various hypotheses have been projected to explain the origin of these factors causing segmental spasm and result in pseudo-obstruction with prominent colonic dilatation. These hypotheses are-

• Parietal and visceral peritoneal inflammation linked to vesicular eruption.
• Viral involvement of the extrinsic autonomic nervous system, either through  infection of anterior horn motor neurons or by involvement of the celiac plexus  ganglion .
• Direct Varicella-Zoster Virus (VZV) injury of both the ENS(Enteric Nervous System-submucosal  and myenteric plexuses) and the colonic muscularis propria. 
• Hemorrhagic infarction of the abdominal sympathetic ganglia as the main mechanism of the colonic pseudo-obstruction .
• VZV injury of the thoracolumbar or sacral lateral columns  may interrupt sacral parasympathetic nerves and subsequently decrease  intestinal contractility.
• Finally, a recent study put forward thoracic herpes zoster may prevent afferent C-fibers  from facilitating gastrointestinal motility (by  tachykinins), with ensuing acute intestinal pseudo-obstruction [26].

Herpetic neuralgia in a dermatomal distribution preceding the rash has long been recognized and noted to antedate the rash by up to 100 days, thereby creating significant diagnostic confusion [27]. The viral spread can involve not just the colon, but also the diaphragm, urinary tract, anus, and abdominal wall, and affect their motor activity [28].

Differential diagnosis includes lumbar hernias, that can occur through the inferior lumbar triangle of Petit or superior triangle of Grynfeelt [10].Thoracoabdominal or truncal neuropathy and lower thoracic motor radiculopathy are rare phenomena that can clinicallypresent as abdominal wall protrusions. The differential diagnosis includes diabetes, herpes zoster, intercostal nerve lesions in surgical or other thoracic procedures, thoracic disk hernia,vertebral metastasis or trauma, clinical events with involvementof abdominal organs (appendicitis or colitis) and thoracic root alteration by another etiology [29].

The overall prognosis for patients with segmental zosterparesis is generally good. According to previous studies,improvement is observed in 55%-85% of patients withsegmental herpes zoster paresis [1,30]. In a large epidemiologic study, Thomas and Howard [1] reported that 75% of patients had full recovery and the other patients showedpartial recovery 1 year from onset. Through our review and analysis of the reported cases that were followed-up, wefound that 79.3% of the patients affected had full clinical recovery of their segmental zoster abdominal paresis in 1 year, with a mean time of 4.9 months and, the remaining 20.7% had partial resolution or no recovery. Finally, 2 of the cases were associated with epidural steroid injections. The patients in these cases did not have dermatomal rash, but were confirmed serologically. The increasing age of the population and increased use of epidural steroid injection may increase the incidence of this complication of HZ [9].