Chronic inflammation of the meninges (pia, arachnoid, and dura) can produce profound neurologic disability and may be fatal if not successfully treated. The causes are varied. Five categories of disease account for most cases of chronic meningitis:
Neurologic manifestations consist of persistent headache with or without stiff neck and hydrocephalus; cranial neuropathies; radiculopathies; and/or cognitive or personality changes (Table 195-1). The diagnosis is usually made when clinical presentation leads the physician to examine CSF for signs of inflammation; on occasion the diagnosis is made when a neuroimaging study shows contrast enhancement of the meninges.
TABLE 195-1Symptoms and Signs of Chronic Meningitis |Favorite Table|Download (.pdf) TABLE 195-1 Symptoms and Signs of Chronic Meningitis
|SYMPTOM ||SIGN |
|Chronic headache ||±Papilledema |
|Neck or back pain/stiffness ||Brudzinski’s or Kernig’s sign of meningeal irritation |
|Change in personality ||Altered mental status—drowsiness, inattention, disorientation, memory loss, frontal release signs (grasp, suck, snout), perseveration |
|Facial weakness ||Peripheral seventh CN paresis |
|Double vision ||Paresis of CNs III, IV, VI |
|Diminished vision ||Papilledema, optic atrophy |
|Hearing loss ||Eighth CN paresis |
|Arm or leg weakness ||Myelopathy or radiculopathy |
|Numbness in arms or legs ||Myelopathy or radiculopathy |
|Urinary retention/incontinence || |
Myelopathy or radiculopathy
Frontal lobe dysfunction (hydrocephalus)
|Clumsiness ||Ataxia |
Two clinical forms exist. In the first, symptoms are chronic and persistent, whereas in the second there are recurrent, discrete episodes with complete resolution of meningeal inflammation between episodes without specific therapy. In the latter group, likely etiologies are herpes simplex virus type 2, chemical meningitis due to leakage from a tumor, a primary inflammatory condition, or drug hypersensitivity.
APPROACH TO THE PATIENT Chronic Meningitis
Once chronic meningitis is confirmed by CSF examination, effort is focused on identifying the cause (Tables 195-2 and 195-3) by (1) further analysis of the CSF, (2) diagnosis of an underlying systemic infection or noninfectious inflammatory condition, or (3) examination of meningeal biopsy tissue.
Proper analysis of the CSF is essential; if the possibility of raised intracranial pressure (ICP) exists, a brain imaging study should be performed before LP. In pts with communicating hydrocephalus caused by impaired resorption of CSF, LP is safe and may lead to temporary improvement. However, if ICP is elevated because of a mass lesion, brain swelling, or a block in ventricular CSF outflow (obstructive hydrocephalus), then LP carries the potential risk of brain herniation. Obstructive hydrocephalus usually requires direct ventricular drainage of CSF.
Contrast-enhanced MRI or CT studies of the brain and spinal cord can identify meningeal enhancement, parameningeal infections (including brain abscess), encasement of the spinal cord (malignancy or inflammation and infection), or nodular deposits on the meninges or nerve roots (malignancy or sarcoidosis). Imaging studies are also useful to ...