The cerebrospinal fluid (CSF) is contained in the brain ventricles and the cranial and spinal subarachnoid spaces. The mean CSF volume is 150 ml, with 25 ml in the ventricles and 125 ml in subarachnoid spaces. CSF is predominantly, but not exclusively, secreted by the choroid plexuses. Brain interstitial fluid, ependyma and capillaries may also play a poorly defined role in CSF secretion. CSF circulation from sites of secretion to sites of absorption largely depends on the arterial pulse wave. Additional factors such as respiratory waves, the subject's posture, jugular venous pressure and physical effort also modulate CSF flow dynamics and pressure. Cranial and spinal arachnoid villi have been considered for a long time to be the predominant sites of CSF absorption into the venous outflow system. Experimental data suggest that cranial and spinal nerve sheaths, the cribriform plate and the adventitia of cerebral arteries constitute substantial pathways of CSF drainage into the lymphatic outflow system. CSF is renewed about four times every 24 hours. Reduction of the CSF turnover rate during ageing leads to accumulation of catabolites in the brain and CSF that are also observed in certain neurodegenerative diseases. The CSF space is a dynamic pressure system. CSF pressure determines intracranial pressure with physiological values ranging between 3 and 4 mmHg before the age of one year, and between 10 and 15 mmHg in adults. Apart from its function of hydromechanical protection of the central nervous system, CSF also plays a prominent role in brain development and regulation of brain interstitial fluid homeostasis, which influences neuronal functioning.

Hydrocephalus in FGFR2-related Crouzon and Pfeiffer syndromes is statistically associated with a small FMA. Hydrocephalus is statistically associated with CTE.

ObjectiveThe efficacy of deep brain stimulation in disorders of consciousness remains inconclusive. We investigated bilateral 30‐Hz low‐frequency stimulation designed to overdrive neuronal activity by dual pallido‐thalamic targeting, using the Coma Recovery Scale Revised (CRS‐R) to assess conscious behavior.MethodsWe conducted a prospective, single center, observational 11‐month pilot study comprising four phases: baseline (2 months); surgery and titration (1 month); blind, random, crossover, 1.5‐month ON and OFF periods; and unblinded, 5‐month stimulation ON. Five adult patients were included: one unresponsive‐wakefulness‐syndrome male (traumatic brain injury); and four patients in a minimally conscious state, one male (traumatic brain injury) and three females (two hemorrhagic strokes and one traumatic brain injury). Primary outcome measures focused on CRS‐R scores. Secondary outcome measures focused notably on baseline brain metabolism and variation in activity (stimulation ON – baseline) using normalized fluorodeoxyglucose positron emission tomography maps. Statistical analysis used random‐effect models.ResultsThe two male patients (one minimally conscious and one unresponsive wakefulness syndrome) showed improved mean CRS‐R scores (stimulation ON vs. baseline), in auditory, visual and oromotor/verbal subscores, and visual subscores respectively. The metabolism of the medial cortices (low at baseline in all five patients) increased specifically in the two responders.InterpretationOur findings show there were robust but limited individual clinical benefits, mainly in visual and auditory processes. Overall modifications seem linked to the modulation of thalamo‐cortico‐basal and tegmental loops activating default mode network cortices. Specifically, in the two responders there was an increase in medial cortex activity related to internal awareness.