Imaging should show an enlargement to at least one of the temporal horns of lateral ventricles, and impingement against the falx cerebri resulting in a callosal angle ≤ 90° on the coronal view, showing evidence of altered brain water content, or normal active flow (which is referred to as "flow void") at the cerebral aqueduct and fourth ventricle.MRI scans are the preferred imaging. The distinction between normal and enlarged ventricular size by cerebral atrophy is difficult to ascertain. Up to 80% of cases are unrecognized and untreated due to difficulty of diagnosis. Imaging should also reveal the absence of any cerebral mass lesions or any signs of obstructions. Although all patients with NPH have enlarged ventricles, not all elderly patients with enlarged ventricles have primary NPH. Cerebral atrophy can cause enlarged ventricles, as well, and is referred to as hydrocephalus ex vacuo. The Miller Fisher test  involves a high-volume lumbar puncture (LP) with removal of 30–50 ml of CSF. Gait and cognitive function are typically tested just before and within 2–3 hours after the LP to assess for signs of symptomatic improvement. The CSF infusion test and the lumbar test are similar tests to Miller Fisher test. The tests have a positive predictive value over 90%, but a negative predictive value less than 50%. The LP should show normal or mildly elevated CSF pressure. CSF should have normal cell contents, glucose levels, and protein levels. Treatment
Ventriculoperitoneal shunts
For suspected cases of NPH, CSF shunting is the first-line treatment.
Prognosis
Hereditary motor and sensory neuropathy are relatively common and are often inherited with other neuromuscular conditions, and these comorbidities cause an accelerated progression of the disease.Most forms of HMSN affect males earlier and more severely than females, but others show no predilection to either sex. HMSN affects all ethnic groups, with the most common forms having no racial predilection, but other recessively inherited forms tending to impact specific ethnic groups. Onset of HMSN is most common in early childhood, with clinical effects occurring before the age of 10, but some symptoms are lifelong and progress slowly. Therefore, these symptoms do not appear until later in life. See also
Hereditary motor and sensory neuropathy with proximal dominance
Charcot–Marie–Tooth disease
Hereditary motor neuropathies
Hereditary sensory and autonomic neuropathies
Spinal muscular atrophies

References
Further reading
Reilly MM (October 2000). "Classification of the hereditary motor and sensory neuropathies". Curr. Opin. Neurol. 13 (5): 561–4. doi:10.1097/00019052-200010000-00009. PMID 11073363. S2CID 43241647. == External links ==