**8. Imaging**

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

**4. Clinical features**

**5. Gait disturbances**

**6. Dementia**

**7. Urinary incontinence**

(e.g., knees, hips, and spine) cause asymmetry.

have found that in patients with NPH, there is reduction in vascular compliance particularly involving superior sagittal sinus. Hakim and Adam's hypothesized [4] that in NPH reduced CSF absorption leads to raised intracranial pressure and over a period leading to compensatory ventricular enlargement. This new intracranial pressure state directs more CSF flow toward the Virchow-Robin spaces and thus into the brain parenchyma [15]. These metabolic and mechanical changes further leads to periventricular damage and raised myelin basic protein (a possible biomarker) elevated in these patients [16]. This leads to tissue compression, white matter ischemia and parenchymal changes characterized by myelin pallor. These changes further lead to periventricular damage, reduced cellular metabolism, clearance of toxins, and their sequel [15, 17]. Studies have shown that following CSF diversion, there is normalization in global brain stiffness and elasticity on magnetic resonance studies [18].

The classical clinical triad of INPH includes gait disturbance, dementia, and urinary incontinence [3–6, 8]. These symptoms are typically insidious in onset, and the patients are in their sixth and eighth decades. These changes occur in presence of ventriculomegaly without much evidence of cortical atrophy on brain imaging [2].

Gait disturbances are the most common initial symptom (present in 90% of the patients) and initially characterized by unsteadiness, frequent falls, slowness of gait, with difficulty initiating and turning, as the disease advances, these transform into magnetic, slow, broad based, and short steps (with preserved arm swing). These gait disturbances are not usually associated with increase in tone, exaggerated reflexes or weakness and usually there is absence of primary sensorimotor deficits, cerebellar dysfunction, or involuntary movements, involving difficulty integrating sensory information about the position of the body in relation to its environment. The impairment should be symmetric unless coexisting musculoskeletal disorders

INPH patients have subcortical frontal dysexecutive syndrome, manifesting as memory impairment, decreased attention, impaired planning, slowness of thought, and apathy. The cognitive findings of NPH reflect involvement of the prefrontal brain structures, similar to a subcortical dementia, with executive dysfunction (e.g., slow processing, and difficulty with problem solving) and memory deficits with poor retrieval and relatively intact recognition memory. Delirium is not typical in NPH and implies the presence of a concomitant disorder or medication side effect.

The urological manifestations include frequency, urgency, and urge incontinence. In a series of 41 patients with possible iNPH, 95% patients had urodynamic evidence of detrusor overactivity [12]. Bladder manifestations in NPH have been attributed to the involvement of sacral fibers of corticospinal pathway. Patients

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The differential diagnosis of NPH other non-treatable causes of dementias and degenerative disorders is extremely for proper selection of potential candidates for CSF diversion. No brain imaging studies are sufficient to diagnose INPH; however ventricular enlargement with appropriate symptoms is necessary to establish a diagnosis of NPH. Combination of imaging modalities and correlation with clinical findings shall help to make a diagnosis of NPH [2]. Evans' index 0.3 or greater suggests significant ventriculomegaly (**Figures 1** and **2**) [19]. Other imaging features include:
