[Progress in diagnosis of and therapy for idiopathic normal-pressure hydrocephalus--Lymphatic drainage of CSF and ISF from the brain: recent concept and hypothesis].

Cerebrospinal fluid (CSF) drains via the cribriform plate and nasal mucosa to cervical lymph nodes. There are no conventional lymphatics in the brain but physiological studies have revealed a substantial and immunologically significant lymphatic drainage from brain to cervical lymph nodes. Interstitial fluid (ISF) and solutes from brain parenchyma drain along capillary and perivascular space of artery, and path through the skull base, then reach to the cervical lymph nodes. CSF and ISF appear to drain by separate routes from the brain, especially in humans. However, there are interrelationships between the two fluid compartments that become more significant when drainage of CSF or ISF is impaired by disease processes. Vessel pulsations appear to be the driving force for the perivascular lymphatic drainage along artery walls, and as vessels stiffen with age, amyloid peptides (Aß) deposit in the drainage pathways as cerebral amyloid angiopathy (CAA). Blockage of lymphatic drainage of ISF and solutes from the brain by CAA may result in loss of homeostasis of the neuronal environment that may contribute to neuronal malfunction and dementia. Such failure of perivascular drainage may associated with the pathoetiology of Alzheimer's disease, cerebral small artery disease and idiopathic normal pressure hydrocephalus (iNPH).

Significance of periventricular hemodynamics in normal pressure hydrocephalus.

To delineate the pathophysiology of periventricular hemodynamics in normal pressure hydrocephalus, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) by using xenon-enhanced computed tomographic scans. Measurements were made on 7 patients in whom normal pressure hydrocephalus after subarachnoid hemorrhage had been confirmed by clinical improvement after shunting. We compared mean CBF values in the white matter and cortex of the frontal, temporal, parietal, and occipital lobes and in the thalamus before and after shunting, with an evaluation of dementia and the extent of ventricular dilation and periventricular lucency on computed tomographic scans. CBF returned to within normal limits in the white matter of the frontal and temporoparieto-occipital lobes. CBF restoration closely correlated with clinical improvement and reduction in ventricular dilation and periventricular lucency. We speculate that ischemia occurs initially in the periventricular white matter as a result of diffused cerebrospinal fluid and then extends of the cortex and to the thalamus, causing a "misery perfusion" state with neuronal dysfunction. Incomplete improvement of dementia and CBF in the cortex and thalamus may be explained by preexisting arteriosclerosis in aged patients, coexisting brain damage caused by subarachnoid hemorrhage and subsequent surgical insult in aneurysm patients, and delayed recovery of cortical function that has been secondarily impaired by the periventricular lesions.

Investigation of normal pressure hydrocephalus by 123I-IMP SPECT.

We evaluated N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) as a method for identifying normal pressure hydrocephalic (NPH) patients eligible for shunting procedures. 123I-IMP SPECT scans were taken before and after cerebrospinal fluid (CSF) taps in NPH cases. Post-subarachnoid hemorrhagic (SAH) patients showed apparent frontal blood flow reduction but non-SAH cases did not. The frontal blood flow increased in comparison with the temporal flow after CSF tapping in SAH cases who benefited most from shunting. Cerebral blood flow study before and after CSF removal is a potential method for classifying NPH patients likely to benefit from the shunting operation.

[Punch drunk syndrome due to repeated karate kicks and punches].

We reported a 39-year-old man with punch drunk syndrome who had cerebellar ataxia, seizure and dementia. CT scan of the brain revealed remarkable atrophy and enlargement of the ventricular system. MRI of the brain showed severe atrophy which was especially evident in the frontal base. On RI cisternography both early ventricular reflux at 3 hours and delayed ventricular stasis at 52 hours were found, which resembled the findings of the normal pressure hydrocephalus. The MRI and RI cisternographic findings suggested that the remarkable brain atrophy and enlargement of the ventricular system were caused by repeated KARATE traumas including minor brain contusion or subarachnoid hemorrhage in the base of the brain, since traumatic brain contusions affect particularly the orbital surfaces of the frontal lobes and the lateral and inferior surfaces of the temporal lobes. Communicating hydrocephalus may be one of the pathogenesis of punch drunk syndrome.