J.	Late stages of certain degenerative diseases (Chap. 38) and of Creutzfeldt-Jakob disease (Chap. 31)
II.        Diseases that cause meningeal irritation and an excess of white blood cells (WBCs) or red blood cells (RBCs) in the CSF, usually without focal or lateralizing cerebral or brainstem signs. CT scanning or MRI (which preferably should precede lumbar puncture) may be normal or abnormal.
A.	Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, and cerebral trauma (Chaps. 33 and 34)
B.	Acute bacterial meningitis (Chap. 31)
C.	Viral meningoencephalitis (Chap. 32)
D.	Neoplastic meningeal infiltration (Chap. 30)
E.	Parasitic meningitis (Chap. 31)
F.		Pituitary apoplexy (Chap. 30)
III. Diseases that cause focal brainstem or lateralizing cerebral signs, with or without changes in the CSF. CT scan and MRI are abnormal.
A.	Hemispheral hemorrhage or massive cerebral infarction (Chap. 33)
B.	Brainstem infarction caused by basilar artery thrombosis or embolism (Chap. 33)
C.	Brain abscess, subdural empyema, herpes encephalitis (Chap. 31)
D.	Epidural and subdural hemorrhage and brain contusion (Chap. 34)
E.	Brain tumor (Chap. 30)
F.	Cerebellar and pontine hemorrhage (Chap. 33)
G.	Multiple focal cerebral lesions that cumulate to cause generalized brain dysfunction: multiple embolic infarction caused by bacterial endocarditis, acute disseminated (postinfectious) encephalomyelitis, intravascular lymphoma, TTP, sagittal sinus thrombosis diffuse fat embolism, and others
Problems in Differential Diagnosis of Coma (Table 16-3)
Using the clinical criteria outlined previously, one can usually ascertain whether a given case of coma falls into one of these three categories. Concerning the group without focal or lateralizing or meningeal signs (which includes most of the metabolic encephalopathies, intoxications, concussion, and postseizure states), it must be kept in mind that residua from previous neurologic disease may confuse the clinical picture. Thus, an earlier hemiparesis from vascular disease or trauma may reassert itself in the course of uremic or hepatic coma with hypotension, hypoglycemia, diabetic acidosis, or following a seizure. In hypertensive encephalopathy, focal signs may also be present. Occasionally, for no understandable reason, one leg may seem to move less, one plantar reflex may be extensor, or seizures may be predominantly or entirely unilateral in a metabolic coma, particularly in the hyperglycemic–hyperosmolar states. Babinski signs and extensor rigidity, conventionally considered to be indicators of structural disease, do sometimes occur in profound intoxications with a number of agents or with hepatic encephalopathy.