Madjid Samii

Disturbances of cerebrospinal fluid flow attributable to arachnoid scarring cause interstitial edema of the cat spinal cord.

OBJECTIVE Spinal arachnoid scarring may be caused by trauma, inflammation, surgery, spinal instability, degenerative diseases, or malformations and may lead to progressive neurological deficits and syringomyelia. We wanted to investigate the effects of focal arachnoid scarring in the cervical spinal canal of cats on pressures in the subarachnoid space and spinal cord tissue, as well as on spinal cord histological features. METHODS Twenty-nine adult cats were used for this study. Nine animals served as control animals, whereas 20 animals received a focal arachnoid scar at C1–C2, which was produced by placement of a kaolin-soaked fibrin sponge on the posterior surface of the spinal cord. After 4 months, pressure recordings above and below the scar, in the subarachnoid space and spinal cord, were performed. Elasticity measurements were performed with small bolus injections. Morphometric analyses of brain and ventricle volumes, sizes of the central canal, and sizes of the perivascular spaces in gray and white matter were also performed. RESULTS No animal developed clinical or neurophysiological evidence of neurological symptoms at any time. In the kaolin-treated group , pressure recordings revealed a significant increase in the subarachnoid pressure at C1, because of the cerebrospinal fluid flow obstruction. Pressure gradients tended to increase at all measuring points. A significant difference was detected between the spinal cord and subarachnoid space at C2, where the intramedullary pressure exceeded the subarachnoid pressure. Elasticity was significantly increased in the spinal cord at C2. Intracranially, no evidence of hydrocephalus was observed. In the spinal cord, perivascular spaces were significantly enlarged in the posterior white matter above the arachnoid scar and in the central gray matter below the area of scarring in the cervical cord. CONCLUSION Arachnoid scarring at C1–C2 produces an interstitial type of edema in the central gray matter below the area of scarring in the cat cervical cord, because of altered cerebrospinal fluid and extracellular fluid flow dynamics. These changes may be interpreted as the initial stage in the development of syringomyelic cavities.

Treatment of Elevated Intracranial Pressure by Infusions of 10% Saline in Severely Head Injured Patients

The management of intracranial pressure (ICP) is a factor in outcome of patients with head trauma. However, recent studies have revealed that the current strategies, which have been applied to control ICP for adequate cerebral perfusion, are unsatisfactory. Against this background, the efficacy of short-term infusions of hypertonic saline on ICP was investigated. In severely head injured (SHI) patients, hypertonic saline (100 ml 10% NaCl) was administered when standard agents (mannitol, sorbitol, THAM) failed in reducing ICP. To evaluate the pressure reduction after saline infusions the resulting ICP relaxations were analysed statistically in respect to the parameters amplitude, duration and dynamic behaviour of the ICP responses. In 42 randomized relaxations, the relative ICP decrease was 43% [28%-58%] (median [interquartile range]). The corresponding pressure drop was 18 mmHg [15-27 mm Hg]. Relaxations lasted for 93 min [64-126 min] and a relative ICP minimum was reached 26 min [12-33 min] after infusion. In the individual cases the temporal course of the parameters amplitude and decline interval depict a tendency toward lower and higher values, respectively, under conditions of a generally increasing ICP. As expected, the infusion of hypertonic saline reduces ICP in patients suffering from SHI. The pressure drop, duration and dynamic behaviour are suspected to depend both on the pressure level to reduce and concomitant medications.

Spontaneous resolution of Chiari I malformation and syringomyelia: case report and review of the literature.

OBJECTIVE AND IMPORTANCE Indications for surgery and the surgical technique of foramen magnum decompression for patients with Chiari I malformation and syringomyelia are controversial issues. This case report supports the view that observation may be adequate for patients without progressive symptoms or with mild clinical symptoms. CLINICAL PRESENTATION A 37-year-old woman presented with a 3-month history of burning dysesthesias and hypesthesia in her right arm. A neurological examination revealed hypesthesia in the right trigeminal distribution. A magnetic resonance imaging scan revealed a Chiari I malformation with syringomyelia between C2 and T2. No hydrocephalus was observed. CLINICAL COURSEBecause the patient’s symptoms regressed spontaneously, surgery was not performed. Thirty-two months after her initial examination, the patient was asymptomatic. A second magnetic resonance imaging scan was obtained, which demonstrated complete spontaneous resolution of the Chiari I malformation and syringomyelia. CONCLUSIONWe attribute the regression of the patient’s symptoms to spontaneous recanalization of cerebrospinal fluid pathways at the foramen magnum, which most likely was due to rupture of the arachnoid membranes that had obstructed cerebrospinal fluid flow.

Occult dysraphism in adulthood: clinical course and management

We present a series of 23 patients with dysraphic malformations and adult onset of symptoms (4 meningoceles, 19 spinal hamartomas). Mean age at presentation was 39±21 years (range 23–67 years). Patients were followed up for a mean period of 19 months (range 0.5–68 months). Only patients with progressive neurological disease were operated on (3 meningoceles and 16 spinal hamartomas). The remaining patients were treated conservatively and continue to be observed clinically. Two of three patients operated for meningoceles improved without recurrence of symptoms. Patients with spinal hamartomas could be divided into two groups according to their main symptom: paraparesis (group A, n = 8) or pain (group B, n = 11). Malformations in group B were typically associated with a tethered cord and tended to be more complex than in group A. The majority of patients in group A showed better long-term results than patients in group B, due to their considerably lower rate of recurrence.

Long-Time in-Vivo Metabolic Monitoring Following Experimental Brain Contusion Using Proton Magnetic Resonance Spectroscopy

In a Sham-controlled study we applied proton magnetic resonance spectroscopy (1H-MRS) at 4.7 T to a model of experimental traumatic brain contusion. The time course of cerebral metabolite changes was monitored in serial investigation in 14 Sprague Dawley rats up to 4 weeks after trauma. 6 animals served as controls. 1H-MRS spectra were acquired from a voxel covering the hippocampus/basal ganglia ipsi and contralateral to the lesion. Metabolites ratios of the injured hemisphere were compared to those ipsilateral in Sham animals and to those of the contralateral side in the trauma animals. NAA/Cr ratio and Glu/Cr ratio, possible markers of neuronal loss, persistently decreased after trauma to a minimum of -40% and -20% versus controls, respectively. One week after trauma Cho/Cr ratio was strongly increased by 73%. This might indicate a high inflammatory activity at that time. Lac/Cr ratio showed long-lasting and continuing increases up to 2000% versus controls as a sign of permanently shifted posttraumatic energy metabolism. 1H-MRS proved to be a useful non-invasive method for in-vivo monitoring of posttraumatic metabolism also in models of brain contusion. In single cases however, accompanying haemorrhage can potentially prevent useful data acquisition.

1H-MR spectroscopic monitoring of posttraumatic metabolism following controlled cortical impact injury: pilot study.

Proton magnetic resonance spectroscopy (1H-MRS) has been increasingly utilised in experimental traumatic brain injury for characterisation of posttraumatic metabolic dysfunction. Following human brain injury pathological findings correlated with outcome measures. Combined with conventional T2-weighted MR imaging MRS is a sensitive tool to evaluate metabolic changes in brain tissue following trauma. Studies have been restricted so far to diffuse axonal injury models and fluid percussion injury. Using a high resolution scanner at 4.7 T, MRI combined with 1H-MRS was applied in a pilot study to the controlled cortical impact injury model of experimental brain contusion (CCII). Eight Sprague-Dawley rats were investigated, of which two served as controls. Four animals were injured 24 h after craniotomy, two investigated at 72 h post craniotomy. MRS/MRI indicated a transient brain oedema development and metabolic changes induced by the craniotomy itself. Following CCII MRI demonstrated that the area of contusion as well as the surrounding brain oedema increased twofold in size within 24 h (p < 0.05). MRS showed an immediate increase of N-acetylaspartate (NAA) and glutamate ipsilateral to the contusion and a drop of NAA on the contralateral side. MRS/MRI investigations in the CCII model demonstrated a potential to further elucidate the pathophysiology following traumatic brain contusion.

Determination of contusion and oedema volume by MRI corresponds to changes of brain water content following controlled cortical impact injury.

The time-course of brain contusion/oedema development as visualised by high-resolution MRI was compared to brain water content following experimental brain contusion. 36 Sprague-Dawley rats underwent Controlled Cortical Impact Injury (CCII), 24 served as controls. In 16 animals serial T2 weighted MRI investigations at 1 h, 4 h, 24 h and 7 d after CCII were performed, in 44 rats hemispheric brain water content was determined at the same time points by wet dry weight method. MRI lesion volume (mm3) and brain water content of injured hemisphere (%) showed for absolute and relative values a strictly parallel course. Significant posttraumatic increases had a maximum at 24 hours. Values on day 7 were below those of 1st h in both methods. The simple non-invasive MRI method quantifies contusion and surrounding penumbra according to elevated tissue water signal. The invasive wet dry weight method quantifies changes of hemispheric brain water content that are likely to take place in contusion core and surrounding penumbra. Therefore, from a theoretical aspect both methods seem comparable. Following experimental brain contusion, the simple MRI method might be an equally sufficient way to describe post-traumatic or post-therapeutic changes of lesion size and brain oedema.

The Pathophysiology of Syringomyelia

We have analyzed more than 500 patients with syringomyelia who were treated within the past 20 years. Either at the craniocervical junction or in the spinal canal, an associated pathology could be found in each patient. Each associated pathology was in close anatomical relation to the syrinx cavity and caused CSF flow obstruction and/or spinal cord tethering to some degree. The best long-term results for treatment of syringomyelia were obtained with successful treatment of the associated pathology.

CSF Dynamics in a Rodent Model of Closed Head Injury

Using ICP measurements and the bolus injection technique dynamic parameters of the cerebrospinal fluid system as there are pressure-volume-index (PVI) and resistance to CSF outflow (Rout) were investigated in a new model of diffuse closed head injury (CHI) in the rat. It was found that in the absence of brain oedema and ICP alterations an increase in PVI and Rout was present in the early (4h) period following head injury. This may be indicative for a reduction in cerebral blood flow and cerebral blood volume, both shown previously to occur after CHI. Furthermore an early impairment of CSF absorption mechanisms is evident. To answer the question, whether bolus injection techniques are advisable for clinical routine and whether results might have a predictive value, further investigations covering longer observation intervals and in the presence of secondary insults to the brain are necessary.

Syringomyelia Associated with Diseases of the Spinal Canal

This chapter will describe the management of patients with disorders of the spinal canal that have caused a syrinx. A major problem in this group may be the exact localization of this underlying pathology. Tumors can be easily visualized with gadolinium-enhanced MRI. All other entities described below may offer diagnostic problems, so that counseling of the patient, indication for surgery, and planning the surgical strategy may be quite difficult. Nevertheless, it is our firm belief that idiopathic syringomyelia does not exist. In each patient, it is possible to identify the cause of syrinx formation. Therefore, every effort should be made to demonstrate the underlying disorder.