Alzheimer’s disease, also called primary degenerative dementia, accounts for more than half of all dementias. It results in memory loss, confusion, impaired judgment, personality changes, disorientation, and loss of language skills; it essentially steals away the patient’s mind. Because this is a primary progressive dementia, the prognosis for a patient with this disease is poor.

The cause of Alzheimer’s disease is unknown; however, several factors are thought to be implicated in this disease. These include neurochemical factors, such as deficiencies in the neurotransmitter acetylcholine, somatostatin, substance P, and norepinephrine; environmental factors; and genetic immunologic factors. Genetic studies show that an autosomal dominant form of Alzheimer’s disease is associated with early onset and early death, accounting for about 100,000 deaths per year. A family history of Alzheimer’s disease and the presence of Down syndrome are two established risk factors. Alzheimer’s disease isn’t exclusive to the elder population; its onset begins in middle age in 1% to 10% of cases.

The brain tissue of patients with Alzheimer’s disease has three hallmark features: neurofibrillary tangles, neuritic plaques, and granulovascular degeneration.

Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig disease, is the most common of the motor neuron diseases that cause muscle atrophy. Symptoms don’t develop until age 50. ALS is a chronic, progressively debilitating disease; ALS patients survive an average of 3 years.

ALS affects about 2 out of 100,000 people per year. The exact cause of ALS is unknown, but about 10% of cases have a genetic component. In these patients, it’s an autosomal dominant trait and affects men and women equally.

Other than a family member affected with the hereditary form, there are no known risk factors.

Classically, ALS affects two or more levels of motor neurons. Affected lower motor neurons lead to progressive musle weakness and atrophy. Stiffness, spasticity, and abnormally active reflexes occur when upper motor neurons are affected.

Guillain-Barré syndrome is an acute, rapidly progressive, and potentially fatal form of polyneuritis that causes muscle weakness and mild distal sensory loss most often in an ascending pattern. Recovery is spontaneous and complete in about 85% of patients within 6 to 12 months, although mild motor or reflex deficits in the feet and legs may persist. The prognosis is best when symptoms clear between 15 and 20 days after onset.

Precisely what causes Guillain-Barré syndrome is unknown, but it may be a cell-mediated immunologic attack on peripheral nerves in response to a virus. The major pathologic effect is segmental demyelination of the peripheral nerves. Because this syndrome causes inflammation and degenerative changes in both the posterior (sensory) and anterior (motor) nerve roots, signs of sensory and motor losses occur simultaneously.

The clinical course of Guillain-Barré syndrome is divided into three phases:

A herniated disk (also known as a herniated nucleus pulposus or a slipped disk) occurs when all or part of the nucleus pulposus—an intervertebral disk’s gelatinous center—extrudes through the disk’s weakened or torn outer ring (anulus fibrosus). The resultant pressure on spinal nerve roots or on the spinal cord itself causes back pain and other symptoms of nerve root irritation.

About 90% of herniations affect the lumbar (L) and lumbosacral spine; 8% occur in the cervical (C) spine and 1% to 2% in the thoracic spine. The most common site for herniation is the L4-L5 disk space. Other sites include L5-S1, L2-L3, L3-L4, C6-C7, and C5-C6.

Lumbar herniation usually develops in people ages 20 to 45 and cervical herniation in those ages 45 or older. Herniated disks affect more men than women.

Herniated disks may result from severe trauma or strain, or they may be related to intervertebral joint degeneration. In an elderly person with degenerative disk changes, minor trauma may cause herniation. A person with a congenitally small lumbar spinal canal or with osteophytes along the vertebrae may be more susceptible to nerve root compression with a herniated disk. This person is also more likely to exhibit neurologic symptoms.

With meningitis, the brain and the spinal cord meninges become inflamed, usually as a result of a viral or a bacterial infection. Such inflammation may involve all three meningeal membranes—the dura mater, the arachnoid, and the pia mater. If the disease is recognized early and the infecting organism responds to antibiotics, the prognosis is good and complications are rare; however, mortality in untreated meningitis is 70% to 100%. The prognosis is worse for infants and the elderly, particularly if antibiotic therapy isn’t started within hours of symptom onset.

Meningitis is almost always a complication of another bacterial infection—bacteremia (especially from pneumonia, empyema, osteomyelitis, or endocarditis), sinusitis, otitis media, encephalitis, myelitis, or brain abscess—usually caused by Neisseria meningitidis, Haemophilus influenzae (in children and young adults), or Streptococcus pneumoniae (in adults). In some cases, a virus is suspected. Meningitis may also follow skull fracture, a penetrating head wound, lumbar puncture, or ventricular shunting procedure. Aseptic meningitis may result from a virus or other organism. Sometimes, no causative organism can be found. Meningitis commonly begins as an inflammation of the pia-arachnoid, which may progress to congestion of adjacent tissues and destruction of some nerve cells.

Multiple sclerosis (MS) is a progressive disease caused by demyelination of the white matter of the brain and spinal cord. With this disease, sporadic patches of demyelination throughout the central nervous system induce widely disseminated and varied neurologic dysfunction. Characterized by exacerbations and remissions, MS is a major cause of chronic disability in young adults.

Prognosis varies; MS may progress rapidly, disabling some patients by early adulthood or causing death within months of onset. However, 70% of patients lead active, productive lives with prolonged remissions.

The exact cause of MS is unknown, but current theories suggest a slow-acting or latent viral infection and an autoimmune response. Other theories suggest that environmental and genetic factors may also be linked to MS. Emotional stress, overwork, fatigue, pregnancy, and acute respiratory tract infections have been known to precede the onset of this illness.