The fluid build-up causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications.

Although the cause of idiopathic (also referred to as primary) NPH remains unclear, it has been associated with various co-morbidities including hypertension, diabetes mellitus, Alzheimer's disease, and hyperlipidemia.

[4] The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problems/gait deviations (note: this diagnosis method is obsolete[5][6]).

Further deficits include difficulty managing finances, taking medications, driving, keeping track of appointments, daytime sleeping, short-term memory impairments, and psychomotor slowing.

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.

The ICP gradually falls but remains slightly elevated, and the CSF pressure reaches a high normal level of 15 to 20 cm H2O.

[12][13] The exact pathogenesis is unknown, but consensus on some mechanisms include:[14] The syndrome is often divided into two groups, primary (also called idiopathic) and secondary, based on cause.

[17] Symptoms of gait deviation, neurological impairment, and urinary incontinence seen in NPH are due to compression of the corresponding regions of the brain that control these functions.

Gait abnormalities are thought to be due to compression of the corticospinal tract fibers in the corona radiata that coordinate motor movements of the legs.

[14] Compression of the brainstem as well as poor perfusion of the periventricular white matter in the prefrontal cortex are also thought to contribute to gait deviations in NPH.

[14][18] Patients with suspected idiopathic NPH should have at least one of the symptoms in Hakim's triad (gait disturbance, urinary incontinence, and cognitive impairment) in addition to ventricular enlargement on neuroimaging.

[22] VP shunt is less likely to be recommended in those who have severe dementia at time of NPH diagnosis, regardless of findings found on MRI or CT.[10][28] Gait symptoms improve in ≥ 85% patients.

[32] Transient reduction in ICP after administration of an acetazolamide bolus has been shown to be a positive predictor for good response after VP shunt placement in NPH patients.

Steroids have demonstrated decreased production of CSF in animal studies on healthy rabbits and dogs, however further testing is required to determine if this is an effective treatment option in humans.

[33][34][35] A trial of triamterene in adults with chronic hydrocephalus has also shown improvement of symptoms within 12 weeks, however further research is needed to support this as a non-surgical option for NPH.

If left untreated, symptoms of gait disturbance, cognitive impairment, and urinary incontinence may continue to worsen and ultimately lead to death.

Hakim was contacted by the family of a 16-year-old male patient who, after suffering from severe head trauma in a motor vehicle accident, remained semi-comatose after surgery to relieve pressure from a subdural hematoma.

Hakim continued to research and work with patients found to have NPH and later published his findings detailing the classic triad of gait disturbance, neurological impairment, and urinary incontinence.