Neuroanatomy Atlas in Clinical Context

60 CHAPTER 4 / MENINGES, CISTERNS, VENTRICLES, AND RELATED HEMORRHAGES

TABLE 4-1 Comparison of Cerebral Versus Spinal Meninges

C erebral

S pinal

Dura

Dura

• Adherent to inner table of skull (no epidural space) • Composed of two fused layers (periosteal, meningeal), which split to form sinuses, and of the dural border cell layer (DBC)

• Separated from vertebrae by epidural space • Composed of meningeal dura only (vertebrae have their own perios teum), and of the DBC layer

Arachnoid (outer part of leptomeninges)

Arachnoid (outer part of leptomeninges)

• Attached to dura in living condition (no preexisting subdural space) • Arachnoid villi (in superior sagittal sinus) • Arachnoid trabeculae in SAS • Subarachnoid space with many cisterns

• Attached to dura in living condition (no preexisting subdural space) • No arachnoid villi • Few or no arachnoid trabeculae but larger arachnoid septae • Subarachnoid space with one main cistern • Intimately adherent to surface of cord • Specializations in the form of denticulate ligaments, filum terminale, and linea splendens • Follows vessels as they pierce the cord Pia (inner part of leptomeninges)

Pia (inner part of leptomeninges) • Intimately adherent to surface of brain • No pial specializations • Follows vessels as they pierce the brain

MENINGITIS, MENINGEAL HEMORRHAGES, AND MENINGIOMA A wide variety of disease processes and lesions may involve the menin ges; only a few examples are mentioned here. Infections of the meninges ( bacterial meningitis ) may be called lep tomeningitis because the causative organisms localize to the SAS and involve the pia and arachnoid . Extension into the dura is called pachy meningitis . A variety of organisms cause bacterial meningitis ; bacteria most commonly associated with certain age groups or with trauma are as follows: neonate = Streptococcus ( S. ) agalactiae , Escherichia ( E. ) coli , Listeria (L.) monocytogenes ; neonate to about 24 months = S. agalactiae , E. coli , Haemophilus (H.) influenzae ; about 2–50 years = S. pneumoniae , Neisseria ( N. ) meningitidis ; about 50 years + = S. pneu moniae , N. meningitidis , L. monocytogenes ; basal skull fracture = S. pneumoniae , H. influenzae ; head trauma = Staphylococcus . The patient becomes acutely ill (i.e., headache , photophobia, confusion , fever , stiff neck [ nuchal rigidity ], stupor ), may have generalized or focal signs/ symptoms, and, if not rapidly treated (with appropriate antibiotics), will likely die. Patients with viral meningitis may become ill over a period of several days, experience headache , confusion , and fever , but most will recover in 1–2 weeks with supportive care. The most common cause of an epidural ( extradural ) hematoma (~85% of cases) is a skull fracture that results in a laceration of a major dural vessel, such as the middle meningeal artery . In approximately 15% of cases, bleeding may come from a venous sinus. The extrava sated blood dissects the dura mater off the inner table of the skull; there is no preexisting cerebral extradural space for the blood to enter. These lesions are frequently large, lens ( lenticular ) shaped, may appear locu lated, and are “ short and thick” compared with subdural hematomas (see Figure 4-4). The fact that epidural hematomas do not cross suture lines correlates with their characteristic shape. The patient may have headache , seizure , vomiting , hyperactive reflexes , or lapse into a coma , and, if the lesion is left untreated, death may result. In some cases, the patient may be unconscious initially , followed by a lucid interval (the patient is wide awake), then subsequently deteriorate rapidly and die; this sequela is called “ talk and die .” Treatment of choice for large lesions is surgical removal of the clot and coagulation of the damaged vessel. Tearing of bridging veins (veins passing from the brain outward through the arachnoid and dura), usually the result of trauma, is a common cause of subdural hematoma . This designation is somewhat

a misnomer because the extravasated blood actually dissects through a specialized, yet structurally weak, cell layer at the dura-arachnoid inter face: the dural border cell layer . There is no preexisting “subdural space” in the normal brain. Acute subdural hematomas , more commonly seen in younger patients, usually are detected immediately or within a few hours after the precipitating incident. Chronic subdural hematomas , usually seen in the elderly or in patients on anticoagulation therapy, are frequently of unknown origin. They may take days or weeks to become symptomatic and, in the process, cause a progressive change in the men tal status of the patient. This lesion appears “long and thin” compared with an epidural hematoma, follows the surface of the brain, and may extend for considerable distances (see Figures 4-4 and 4-5). Treatment is surgical evacuation (for larger or acute lesions) or close monitoring for small, asymptomatic, or chronic lesions. The most common cause of subarachnoid hemorrhage is trauma. In approximately 75% to 80% of patients with spontaneous (nontrau matic) subarachnoid hemorrhage , the precipitating event is rupture of an intracranial aneurysm. Symptomatic bleeding from an arteriovenous malformation occurs in ~5% of cases. Blood collects in and percolates through the SAS and cisterns (see Figure 4-7). Sometimes, the deficits seen (assuming the patient is not in a coma) may be a clue as to loca tion, especially if cranial nerves are nearby. Onset is sudden; the patient complains of a sudden and excruciatingly painful headache (“the worst of my life,” or “thunderclap”) and may remain conscious , may become lethargic and disoriented , or may be comatose . Treatment of an aneu rysm is to surgically separate the sac of the aneurysm from the parent vessel (by surgical clip or endovascular coil), if possible, and to protect against the development of vasospasm. Tumors of the meninges ( meningiomas ) are classified in different ways, but usually they arise from arachnoid cap/stem cells (a small number are dural in origin) around the villi or at places where ves sels or cranial nerves penetrate the dura-arachnoid. These tumors may present with signs/symptoms based on their location and size. They grow slowly (symptoms may develop almost imperceptibly over years), are histologically benign , may result in hyperostosis of the overlying skull, and frequently contain calcifications . In decreasing order, meningiomas are found in the following locations: parasagittal area + falx cerebri (together 29%), convexity 15%, sellar 13%, sphe noid ridge 12%, and olfactory groove 10%. Treatment is primarily by surgical removal, although in some cases meningiomas are treated by radiotherapy.

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