The gait deviation can be classified as mild, marked, or severe: "marked" is when the patient has difficulty walking because of considerable instability; "severe" is when it is not possible for the patient to walk without aids (such as a cane or a wheeled walker).Dementia presents as progressive cognitive impairment which is present in 60% of patients at time of treatment. This is caused by distortions predominantly at the frontal lobe and the subcortex. Initial deficits involve planning, organization, attention, and concentration. Further deficits include difficulty managing finances, taking medications, driving, keeping track of appointments, daytime sleeping, short-term memory impairments, and psychomotor slowing. Late stage features include apathy, reduced drive, slowed thinking, and reduced speech. Urinary incontinence appears late in the illness, and is present in 50% of patients at time of treatment. Urinary dysfunction begins as increased frequency often at night, and progresses to urge incontinence and permanent incontinence. Pathogenesis
Every day, the body makes roughly 600–700 ml of CSF, and about the same amount is reabsorbed into the bloodstream. Hydrocephalus is due to an imbalance between the amount of fluid produced and its absorption rate. Enlarged ventricles put increased pressure on the adjacent cortical tissue and cause myriad effects in the patient, including distortion of the fibers in the corona radiata. This leads to an increase in intracranial pressure (ICP). The ICP gradually falls, but still remains slightly elevated, and the CSF pressure reaches a high normal level of 150 to 200 mm H2O. Measurements of ICP, therefore, are not usually elevated.
Normal-pressure hydrocephalus (NPH), also called malresorptive hydrocephalus, is a form of communicating hydrocephalus in which excess cerebrospinal fluid (CSF) occurs in the ventricles, and with normal or slightly elevated cerebrospinal fluid pressure. As the fluid builds up, it causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications. The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problens/gait deviations (note: this diagnosis method is obsolete). The disease was first described by Salomón Hakim and Adams in 1965.The treatment is surgical placement of a ventriculoperitoneal shunt to drain excess CSF into the lining of the abdomen where the CSF will eventually be absorbed. NPH is often misdiagnosed as other conditions including Parkinsons disease (due to gait) or Alzheimers disease (due to cognitive dysfunction). Signs and symptoms
NPH exhibits a classic triad of clinical findings (known as the Adams triad or Hakims triad). The triad consists of walking difficulty, reduced attention span, and urinary frequency or incontinence. The triad is considered obsolete for diagnosis purposes and newer guidelines are available.Gait deviations are present in nearly all patients and usually the first symptom. This is caused by expansion of the lateral ventricles to impinge on the corticospinal tract motor fibers. The typical gait abnormality in NPH is a broad-based, slow, short-stepped, "stuck to the floor", or "magnetic" movement. The gait abnormalities in NPH may bear resemblance to a gait associated with Parkinsons disease.