Neurological observations are an essential aspect of assessment in patients with altered mental status and require the nurse to collect and analyse information using a validated assessment tool. Assessing a patient's pupil size and response is also an important element of a neurological assessment. This article summarises the pathophysiology of raised intracranial pressure and lists some of the conditions that may contribute to an alteration in a patient's mental status. The article details the use of two commonly used neurological assessment tools and the assessment of a patient's pupil size and response. The author also considers the challenges related to accurate recording of neurological observations.

Blood dynamically and richly supplies the cerebral tissue via microvessels invested in pia matter perforating the cerebral substance. Arteries penetrating the cerebral substance derive an investment from one or two successive layers of pia mater, luminally apposed to the pial-glial basal lamina of the microvasculature and abluminally apposed to a series of aquaporin IV-studded astrocytic end feet constituting the soi-disant glia limitans. The full investment of successive layers forms the variably continuous walls of the periarteriolar, pericapillary, and perivenular divisions of the perivascular fluid compartment. The pia matter disappears at the distal periarteriolar division of the perivascular fluid compartment. Plasma from arteriolar blood sequentially transudates into the periarteriolar division of the perivascular fluid compartment and subarachnoid cisterns in precession to trickling into the neural interstitium. Fluid from the neural interstitium successively propagates into the venules through the subarachnoid cisterns and perivenular division of the perivascular fluid compartment. Fluid fluent within the perivascular fluid compartment flows gegen the net direction of arteriovenular flow. Microvessel oscillations at the central tendency of the cerebral vasomotion generate corresponding oscillations of within the surrounding perivascular fluid compartment, interposed betwixt the abluminal surface of the vessels and internal surface of the pia mater. The precise microanatomy of this most fascinating among designable spaces has eluded the efforts of various investigators to interrogate its structure, though most authors non-consensusly concur the investing layers effectively and functionally segregate the perivascular and subarachnoid fluid compartments. Enlargement of the perivascular fluid compartment in a variety of neurological disorders, including senile dementia of the Alzheimer's type and cerebral small vessel disease, may alternately or coordinately constitute a correlative marker of disease severity and a possible cause implicated in the mechanistic pathogenesis of these conditions. Venular pressures modulating oscillatory dynamic flow within the perivascular fluid compartment may similarly contribute to the development of a variety among neurological disorders. An intimate understanding of subtle features typifying microanatomy and microphysiology of the investing structures and spaces of the cerebral microvasculature may powerfully inform mechanistic pathophysiology mediating a variety of neurovascular ischemic, neuroinfectious, neuroautoimmune, and neurodegenerative diseases.

Headaches attributed to low cerebrospinal fluid (CSF) pressure are described as orthostatic headaches caused by spontaneous or secondary low CSF pressure or CSF leakages. Regardless of the cause, CFS leaks may lead to intracranial hypotension (IH) and influence cerebral blood flow (CBF). When CSF volume decreases, a compensative increase in intracranial blood volume and cerebral vasodilatation occurs. Sinking of the brain and traction on pain-sensitive structures are thought to be the causes of orthostatic headaches. Although there are many studies concerning CBF during intracranial hypertension, little is known about CBF characteristics during low intracranial pressure. The aim of this review is to examine the relationship between CBF, CSF, and intracranial pressure in headaches assigned to low CSF pressure.

Although decompressive surgery following traumatic spinal cord injury (TSCI) is recommended, adequate surgical decompression is rarely verified via imaging. We utilized magnetic resonance imaging (MRI) to analyze the rate of spinal cord decompression after surgery. Pre-operative (within 8 h of injury) and post-operative (within 48 h of injury) MRI images of 184 motor complete patients (American Spinal Injury Association Impairment Scale [AIS] grade A = 119, AIS grade B = 65) were reviewed to verify spinal cord decompression. Decompression was defined as the presence of a patent subarachnoid space around a swollen spinal cord. Of the 184 patients, 100 (54.3%) underwent anterior cervical discectomy and fusion (ACDF), and 53 of them also underwent laminectomy. Of the 184 patients, 55 (29.9%) underwent anterior cervical corpectomy and fusion (ACCF), with (26 patients) or without (29 patients) laminectomy. Twenty-nine patients (16%) underwent stand-alone laminectomy. Decompression was verified in 121 patients (66%). The rates of decompression in patients who underwent ACDF and ACCF without laminectomy were 46.8% and 58.6%, respectively. Among these patients, performing a laminectomy increased the rate of decompression (72% and 73.1% of patients, respectively). Twenty-five of 29 (86.2%) patients who underwent a stand-alone laminectomy were found to be successfully decompressed. The rates of decompression among patients who underwent laminectomy at one, two, three, four, or five levels were 58.3%, 68%, 78%, 80%, and 100%, respectively (p < 0.001). In multi-variate logistic regression analysis, only laminectomy was significantly associated with successful decompression (odds ratio 4.85; 95% confidence interval 2.2-10.6; p < 0.001). In motor complete TSCI patients, performing a laminectomy significantly increased the rate of successful spinal cord decompression, independent of whether anterior surgery was performed.

Trauma to the brain from injury or illness can cause sustained, raised intracranial pressure. In such patients, neurological observations are a fundamental aspect of nursing care and the ability to make and record such observations accurately is an essential nursing skill. Neurological observations are a collection of information on the function and integrity of a patient's central nervous system-the brain and and spinal cord. This article will discuss the tools used in their observation, including the Glasgow Coma Scale tool, pupillary response, and limb power observations, and provide a 'how-to' guide on neurological observations.

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiologic condition encountered in many different clinical settings; it generally occurs in the context of hypertensive crisis, immunosuppressive therapy, or autoimmune diseases. It is characterized by headache, stupor, seizures, and visual alterations. Magnetic resonance imaging findings include white matter changes preferentially in the parieto-occipital regions. Although pathogenesis is not fully elucidated, vasoconstriction and brain hypoperfusion seem to be the cause of brain ischemia and vasogenic edema. Cerebrospinal fluid hypotension is also a reported plausible pathogenic mechanism.

We present a case of PRES following laminectomy and fixation for L4-5 lumbar stenosis and spondylolisthesis. The patient presented with status epilepticus immediately after surgery that lasted 5 days. Brain magnetic resonance imaging showed fluid attenuated inversion recovery and T2 hyperintensities in the bilateral parietal and occipital lobes and external capsules. On the basis of postoperative lumbar images, we hypothesized that an unnoticed cerebrospinal fluid leak might have contributed to development of PRES. The patient developed multiple postoperative complications but ultimately recovered after treatment for severe hypertension and seizures.

Prompt recognition and treatment of this potentially life-threatening syndrome is necessary to increase the likelihood of favorable outcome. Spinal surgeons need to be aware of the possibility of neurologic deterioration after spinal surgery and be alert about the occurrence of a dural leak, either recognized or unnoticed, as the plausible mechanism triggering PRES.