A 50-year-old immunocompetent Hispanic male patient presented in April 2017 to the California Hospital Medical Center in Los Angeles with dizziness, nausea, headache, and a 2-week history of flu-like symptoms. Routine chest radiograph showed no abnormalities. Suspected bacterial meningitis was treated with vancomycin and ceftriaxone. Neurological examination revealed cranial nerves II through XII intact, no sensory or motor deficits, stable gait, DTRs 2+ bilaterally, and a negative Babinski sign. Serum lab results showed white blood cell count of 17,000/mm3. The patient had lumbar puncture done which revealed xanthochromic CSF fluid with a lymphocytic pleocytosis: WBC count of 234/mm3 (94% lymphocytes), glucose of 17 mg/dL, and CSF protein of 90 mg/dL. CT of the head showed ventricular enlargement and hydrocephalus with basal cistern patterns, but he did not require a shunt. Also, mild volume loss with small chronic ischemic disease was noted. Considering the CT of the head, dexamethasone was initiated, and the evaluation to establish the etiology of the meningitis was performed. Initial negative laboratory results were as follows: influenza A or B virus; CSF cryptococcal antigen; HIV-1/2 Ag/Ab screen; blood cultures; CSF cultures; and PCR for Mycobacterium tuberculosis. However, 6 days later the patient's condition worsened, and he was transferred to the ICU. The patient was not responding to the antibiotic and corticosteroid treatment, and his condition deteriorated rapidly over the next few days. Coccidioidal meningitis was confirmed with CSF Coccidioides complement fixing antibody titer of 1:2048. Treatment with IV fluconazole 1200 mg daily was then initiated. Neurological assessment demonstrated altered mental status; the patient was alert, oriented x1, responding to his name only, unable to follow commands, was able to move all extremities but had decreased grip strength bilaterally, held arms in flexion, and had difficulty feeding himself. Blunted left nasolabial fold was noted as a new manifestation. CT of the head demonstrated slightly improved hydrocephalus when compared to the previous exam. MRI of the brain showed meningeal enhancement in the basilar cisterns suggestive of basilar meningitis or a granulomatous process and 9 mm acute infarct in the right globus pallidus. Several days after initiation of fluconazole, follow-up neurological exam exhibited no improvement; the patient's motor strength gradually decreased with intact sensation and withdrawal to stimuli. MRI of C-spine (Figure 1) and T-spine without contrast revealed areas of signal changes in the cord secondary to myelitis and inflammation. MRI of L-spine without contrast showed crowding of the nerve roots in the lower lumbar spinal canal, suggestive of arachnoiditis, and explained the cause of the patient's significant neurological decline. The patient's motor strength decreased to 3/5 in proximal upper extremities and 0/5 in distal upper extremities with very poor hand grasp bilaterally. The patient lost bladder control, and his lower extremities were paralyzed completely even though his mentation improved.