Tuberculous meningoencephalitis (TM) is an acute progressive form of tuberculosis (TB), which accounts for approximately 2% of all infectious diseases affecting the central nervous system [1]. To reduce the risk of mortality and serious complications from TM, a precise diagnosis and prompt prescription of intense treatment are of vital importance [2]. The epidemiology, clinical signs, and diagnosis of TB are well established, but several atypical forms of tuberculous spinal arachnoiditis can easily be misdiagnosed [3].

Arachnoiditis is a rare disorder that causes chronic pain and may even result in long-term disability with paraplegia. Its pathophysiology includes the invasion of fibrinous and oligocellular exudates that result from inflammatory processes in the pia arachnoid layer, causing adhesion of the nerve roots to the arachnoid lining of the meninges. These inflammatory processes may result from spinal trauma, neoplasms, surgery, lumbar puncture, or spinal infections, including TB [4,5].

Here, we report a rare case of TM with cauda equina arachnoiditis diagnosed by magnetic resonance imaging (MRI) and electrodiagnostic study. A loss of sphincter control and weakness of the lower extremities were improved with corticosteroid and anti-TB medication. Several atypical forms of tuberculous spinal arachnoiditis exist, making the diagnosis confusing. Unlike usual TM, this case had symptoms of urinary incontinence and stool incontinence, leading to the suspicion of cauda equina syndrome (CES). We illustrate the difficulties in diagnosing this disease and the necessity of electrodiagnostic studies for diagnosing TM arachnoiditis-induced CES with bladder and bowel dysfunction.

A 26-year-old otherwise healthy male patient experienced fever, headache, and gait disturbance accompanied by bladder disturbances with constipation. The urinary and fecal incontinence progressed, and he was unable to control the anal sphincter. As the symptoms worsened for 1 week, he was transferred to the emergency department of a tertiary training hospital.

Brain MRI revealed meningeal enhancement at the basal meninges. The adenosine deaminase (ADA) level in the cerebrospinal fluid (CSF) was elevated at 22 U/L. Both serum and CSF rapid plasma reagents for syphilis were negative. On the basis of the brain MRI and ADA results, the patient was diagnosed with TM. Intravenous methylprednisolone was initiated at 1 g daily for 5 days, followed by oral prednisolone at 60 mg for another 5 days, with a gradual tapering of the dose over 20 more days. The patient was also given TB medication, including isoniazid (150 mg daily), rifampin (300 mg daily), ethambutol (1,200 mg daily), and pyrazinamide (500 mg daily).

When the patient was medically stable 1 month after the onset of illness, he was transferred to our rehabilitation department. His vital signs were normal upon admission, with no fever, and he demonstrated intact cognitive and cranial nerve function. He showed normal muscle tone in the upper extremities, but weakness in the lower extremities made him unable to stand. He presented grade 2 muscle weakness according to the Medical Research Council (MRC) scale.

The patient remained incontinent for urine and feces. His self-voiding volume was as little as 50 cc, so he started self-catheterization. A urodynamic study revealed an areflexic neurogenic bladder. We added bethanechol chloride and tamsulosin, as the volume of residual urine remained as high as 300 cc. Self-defecation was impossible. Fecal incontinence and constipation continued, so we used a rectal suppository every other day.

Since bladder and bowel impairment is not common in TM, we decided to perform a physical examination for CES, spine MRI, and electrodiagnosis to identify the cause. A sensory examination was normal in temperature and proprioception except in the perianal area. The anal sphincter tone was hypotonic, and the bulbocavernosus reflex (BCR) was equivocal according to our physical examination. MRI of the lumbar spine found an arachnoid cyst at the L4/5 through L5/S1 level (Fig. 1).

An electrodiagnostic study was performed 2 months after onset. A nerve conduction study of both the motor and sensory nerve fibers of the bilateral lower extremities showed acceptable amplitude and velocity (Table 1), while needle electromyography (EMG) recordings suggested bilateral diffuse lumbar and lumbosacral polyradiculopathy. Abnormal spontaneous activity was noted in the muscles, including the paraspinals, iliopsoas, gluteus maximus, tensor fascia latae, vastus medialis, tibialis anterior, gastrocnemius, extensor hallucis longus, anal sphincter, and bulbocavernosus. The sensory-evoked potential (SEP) of the pudendal nerve was prolonged. The bulbocavernosus reflex latency (BCRL) was prolonged, indicating an incomplete sacral reflex arc lesion, such as a cauda equina injury (Table 2).

The patient continued to be treated with antitubercular medication and underwent physical rehabilitation. One month after admission to our rehabilitation center, he demonstrated improved lower extremity muscle power, with the MRC grade improving from 2 to 4. He was able to walk without support but remained incontinent for urine and feces.

Written informed consent by the patients was waived due to a retrospective nature of our study.

Adhesive arachnoiditis is a rare condition that has been infrequently described in the medical literature. Therefore, the true incidence of the disease is unknown, and its numbers may be quite underestimated due to the omission of subclinical cases or the presentation of cases that explain it as the cause of paralysis in patients with other, undiagnosed causes of spinal stenosis. The etiology of adhesive arachnoiditis is heterogeneous. The most common causes include infection (bacteria, TB, and syphilis), trauma, tumor, and contamination of a cyst by intraspinal injections [6,7].

The clinical symptoms of arachnoiditis of the lumbar spine are low back pain, sudden paresthesia of both legs, and bladder and bowel sphincter dysfunction. These can be symptoms of compression of the nerve roots of the cauda equina, so they may be explained by other spinal pathologies, such as CES and inflammatory neuropathy. In a clinical review of 63 patients, 83% had lumbar-sacral arachnoiditis, while the rest had thoracic or cervical forms [8].

MRI plays an important role in diagnosing adhesive arachnoiditis, as its sensitivity is about 92%, and its specificity reaches 100% [9]. The most common MRI abnormalities are the presence of arachnoid cysts, displacement and anchoring, swelling of the spinal cord, as well as atrophy of the spinal cord with syrinx formation [6].

In our case, a young man presented with fever, bilateral leg weakness, gait disturbance, and urinary and fecal incontinence. TM was diagnosed, as brain MRI showed meningeal enhancement at the basal meninges and an increased level of ADA in the CSF. The patient started pulse treatment of high-dose intravenous corticosteroid therapy and antituberculosis therapy with a combination of drugs. As urinary and fecal incontinence is not a common symptom of TM, we obtained an MRI scan of the lumbar spine that revealed an arachnoid cyst at the L4/5 through L5/S1 level. A physical examination (anal tone) and manual BCR testing were used as early tools for identifying CES. As the MRI findings and physical examination suggested cauda equina nerve root compression, we performed nerve conduction, EMG, and pudendal SEP and BCRL studies. The report indicated bilateral diffuse lumbar and lumbosacral polyradiculopathy, including abnormal spontaneous activity in all key lower extremity muscles and the anal sphincter, as well as prolonged pudendal SEP and BCRL, showing an incomplete sacral reflex arc lesion, such as CES.

The patient in the present case had CES symptoms, but this diagnostic possibility was difficult to recognize, as TM-associated CES is very rare. In New Zealand, among 104 patients with certain or likely TM, myeloradiculopathy that caused sphincter dysfunction, weakness of the lower extremities, and loss of sensation occurred in only three patients [10]. Several atypical forms of tuberculous spinal arachnoiditis that give rise to confusing diagnoses are well known. Anatomically, an L4/5 and L5/S1 arachnoid cyst can cause saddle-type anesthesia, sphincter dysfunction, and reflex and BCR reductions, as observed in this patient. EMG is considered an important dynamic diagnostic procedure for radiculopathy and peripheral neuropathy in TM [11]. In this case, a nerve conduction study, EMG, BCRL, and pudendal SEP helped not only to diagnose CES but also to determine the severity of the condition following the presence of sphincter dysfunction. A previous study showed significant differences in BCR and pudendal SEP outliers in CES patients compared to the control group, confirming that these two parameters have diagnostic value for CES [12].

In conclusion, lumbar arachnoiditis-induced by TM is a rare clinical entity and warrants a heightened index of suspicion. It is a condition with various etiologies and symptoms that can lead to potentially serious and irreversible disorders. This case illustrates the usefulness of nerve conduction, EMG, and pudendal SEP and BCRL studies in diagnosing CES induced by TB arachnoiditis. CES should be suspected in TM patients with bladder and bowel incontinence. Patients with TM rarely develop bladder and bowel impairment, which led to the suspicion of CES in this case. The patient had painless urinary retention with overflow incontinence and loss of the signal to void. MRI and electrodiagnosis may be helpful in the diagnostic process. Through CES diagnosis, rapid self-catheterization was performed to ensure that no residual volume was left after voiding. Pelvic floor exercises can assist in the control of bowel movements. In addition, pressure ulcers can be prevented by repositioning with saddle anesthesia. It should also be emphasized that non-discogenic cauda equina disorder caused by TB arachnoiditis can show rapid improvement of lower limb weakness, but bladder bowel problems may be long-lasting.