Novel clinicopathological characteristics differentiate dementia with Lewy bodies from Parkinson's disease dementia.

Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) known as Lewy body dementias have overlapping clinical and neuropathological features. Neuropathology in both includes combination of Lewy body and Alzheimer's disease (AD) pathology. Cerebral amyloid angiopathy (CAA), often seen in AD, is increasingly recognized for its association with dementia. AIMS: This study investigated clinical and neuropathological differences between DLB and PDD. METHODS: 52 PDD and 16 DLB cases from the Queen Square Brain Bank (QSBB) for Neurological disorders were included. Comprehensive clinical data of motor and cognitive features were obtained from medical records. Neuropathological assessment included examination of CAA, Lewy body and AD pathology. RESULTS: CAA was more common in DLB than in PDD (P = 0.003). The severity of CAA was greater in DLB than in PDD (P = 0.009), with significantly higher CAA scores in the parietal lobe (P = 0.043), and the occipital lobe (P = 0.008), in DLB than in PDD. The highest CAA scores were observed in cases with APOE ε4/4 and ε2/4. Survival analysis showed worse prognosis in DLB, as DLB reached each clinical milestone sooner than PDD. Absence of dyskinesia in DLB is linked to the significantly lower lifetime cumulative dose of levodopa in comparison with PDD. CONCLUSIONS: This is the first study which identified prominent concurrent CAA pathology as a pathological substrate of DLB. More prominent CAA and rapid disease progression as measured by clinical milestones distinguish DLB from PDD.

Morbidity of redo surgery for thyroid disease.

OBJECTIVE: Redo thyroid surgery is generally associated with more complications than firsthand surgery. The actual study reports a single center experience of redo thyroid surgery compared to primary bilateral thyroidectomy. STUDY DESIGN: Mono institutional retrospective study. METHODS: Institutional review of redo thyroid surgery patients (Group 2 : completion thyroidectomy and Group 3 : thyroidectomy for recurrent thyroid diseases) compared to Group 1 : primary bilateral thyroidectomy operated on during the same time interval. RESULTS: Demographic characteristics were not different between groups. Substernal extension and hyperthyroidism were more frequent in group 1. Weight of the resected thyroid gland was lower in groups 2 and 3. Incidence of transient hypocalcemia, permanent hypoparathyroidism, transient and permanent recurrent laryngeal palsy was not different between the groups. Hematoma occurred in 5% of cases in the 3 groups and postoperative length of stay was 1 day in 92% of cases of the 3 groups. CONCLUSIONS: Redo thyroid surgery can be performed with no excess morbidity provided strict selection criteria, having reoperation in mind while performing firsthand intervention.

Human thymic MR1-restricted MAIT cells are innate pathogen-reactive effectors that adapt following thymic egress.

Human mucosal-associated invariant T (MAIT) cells express the semi-invariant T-cell receptor (TCR) Vα7.2 and are restricted by the major histocompatibility complex-Ib molecule MR1. While MAIT cells share similarities with other innate T cells, the extent to which MAIT cells are innate and their capacity to adapt is unknown. We evaluated the function of Vα7.2(+) T cells from the thymus, cord blood, and peripheral blood. Although antigen-inexperienced MAIT cells displayed a naïve phenotype, these had intrinsic effector capacity in response to Mycobacterium tuberculosis (Mtb)-infected cells. Vα7.2(+) effector thymocytes contained signal joint TCR gene excision circles (sjTRECs) suggesting limited replication and thymic origin. In evaluating the capacity of Mtb-reactive MAIT cells to adapt, we found that those from the peripheral blood demonstrated a memory phenotype and had undergone substantial expansion, suggesting that they responded to antigenic stimulation. MAIT cells, an evolutionarily conserved T-cell subset that detects a variety of intracellular infections, share features of innate and adaptive immunity.

Changes in glial glutamate transporters in human epileptogenic hippocampus: inadequate explanation for high extracellular glutamate during seizures.

Temporal lobe epilepsy (TLE) with hippocampal sclerosis is associated with high extracellular glutamate levels, which could trigger seizures. Down-regulation of glial glutamate transporters GLAST (EAAT1) and GLT-1 (EAAT2) in sclerotic hippocampi may account for such increases. Their distribution was compared immunohistochemically in non-sclerotic and sclerotic hippocampi and localized only in astrocytes, with weaker immunoreactivity for both transporters in areas associated with pronounced neuronal loss, especially in CA1, but no decrease or even an increase in areas with less neuronal loss, like CA2 and the subiculum in the sclerotic group. Such compensatory changes in immunoreactivity may account for the lack of differences between the groups in immunoblot studies as blots show the average concentrations in the samples. These data suggest that differences in glial glutamate transporter distribution between the two groups of hippocampi may be an insufficient explanation for the high levels of extracellular glutamate in sclerotic seizure foci observed through in vivo dialysis studies.

Loss of glutamine synthetase in the human epileptogenic hippocampus: possible mechanism for raised extracellular glutamate in mesial temporal lobe epilepsy.

BACKGROUND: High extracellular glutamate concentrations have been identified as a likely trigger of epileptic seizures in mesial temporal lobe epilepsy (MTLE), but the underlying mechanism remains unclear. We investigated whether a deficiency in glutamine synthetase, a key enzyme in catabolism of extracellular glutamate in the brain, could explain the perturbed glutamate homoeostasis in MTLE. METHODS: The anteromedial temporal lobe is the focus of the seizures in MTLE, and surgical resection of this structure, including the hippocampus, leads to resolution of seizures in many cases. By means of immunohistochemistry, western blotting, and functional enzyme assays, we assessed the distribution, quantity, and activity of glutamine synthetase in the MTLE hippocampus. FINDINGS: In western blots, the expression of glutamine synthetase in the hippocampus was 40% lower in MTLE than in non-MTLE samples (median 44 [IQR 30-58] vs 69 [56-87]% of maximum concentration in standard curve; p=0.043; n=8 and n=6, respectively). The enzyme activity was lower by 38% in MTLE vs non-MTLE (mean 0.0060 [SD 0.0031] vs 0.0097 [0.0042] U/mg protein; p=0.045; n=6 and n=9, respectively). Loss of glutamine synthetase was particularly pronounced in areas of the MTLE hippocampus with astroglial proliferation, even though astrocytes normally have high content of the enzyme. Quantitative immunoblotting showed no significant change in the amount of EAAT2, the predominant glial glutamate transporter in the hippocampus. INTERPRETATION: A deficiency in glutamine synthetase in astrocytes is a possible molecular basis for extracellular glutamate accumulation and seizure generation in MTLE. Further studies are needed to define the cause, but the loss of glutamine synthetase may provide a new focus for therapeutic interventions in MTLE.

Disruption of inhibition in area CA1 of the hippocampus in a rat model of temporal lobe epilepsy.

Previous studies have revealed a loss of neurons in layer III of the entorhinal cortex (EC) in patients with temporal lobe epilepsy. These neurons project to the hippocampus and may activate inhibitory interneurons, so that their loss could disrupt inhibitory function in the hippocampus. The present study evaluates this hypothesis in a rat model in which layer III neurons were selectively destroyed by focal injections of the indirect excitotoxin, aminooxyacetic acid (AOAA). Inhibitory function in the hippocampus was assessed by evaluating the discharge of CA1 neurons in response to stimulation of afferent pathways in vivo. In control animals, stimulation of the temporo-ammonic pathway leads to heterosynaptic inhibition of population spikes generated by subsequent stimulation of the commissural projection to CA1. This heterosynaptic inhibition was substantially reduced in animals that had received AOAA injections 1 mo previously. Stimulation of the commissural projection also elicited multiple population spikes in CA1 in AOAA-injected animals, and homosynaptic inhibition in response to paired-pulse stimulation of the commissural projection was dramatically diminished. These results suggest a disruption of inhibitory function in CA1 in AOAA-injected animals. To determine whether the disruption of inhibition occurred selectively in CA1, we assessed paired-pulse inhibition in the dentate gyrus. Both homosynaptic inhibition generated by paired-pulse stimulation of the perforant path, and heterosynaptic inhibition produced by activation of the commissural projection to the dentate gyrus appeared largely comparable in AOAA-injected and control animals; thus abnormalities in inhibitory function following AOAA injections occurred relatively selectively in CA1. Electrolytic lesions of the EC did not cause the same loss of inhibition as seen in animals with AOAA injections, indicating that the loss of inhibition in CA1 is not due to the loss of excitatory driving of inhibitory interneurons. Also, electrolytic lesions of the EC in animals that had been injected previously with AOAA had little effect on the abnormal physiological responses in CA1, suggesting that most alterations in inhibition in CA1 are not due to circuit abnormalities within the EC. Comparisons of control and AOAA-injected animals in a hippocampal kindling paradigm revealed that the duration of afterdischarges elicited by high-frequency stimulation of CA3, and the number of stimulations required to elicit kindled seizures were comparable. Taken together, our results reveal that the selective loss of layer III neurons induced by AOAA disrupts inhibitory function in CA1, but this does not create a circuit that is more prone to at least one form of kindling.

Ibotenate injections into the pre- and parasubiculum provide partial protection against kainate-induced epileptic damage in layer III of rat entorhinal cortex.

PURPOSE: A loss of neurons in layer III of the entorhinal cortex (EC) is often observed in patients with temporal lobe epilepsy and in animal models of the disorder. We hypothesized that the susceptibility of layer III of the EC to prolonged seizure activity might be mediated by excitatory afferents originating in the presubiculum. METHODS: Experiments were designed to ablate the presubiculum unilaterally by focal ibotenate injections and to evaluate the effect of this deafferentation on the vulnerability of EC layer III neurons to the chemoconvulsant kainate (injected systemically 5 days later). RESULTS: After treatment with kainate, 11 of the 15 rats preinjected with ibotenate showed clear-cut, partial neuroprotection in layer III of the EC ipsilateral to the ibotenate lesion. Serial reconstruction of the ibotenate-induced primary lesion revealed that entorhinal neurons were protected only in animals that had lesions in the pre- and parasubiculum, especially in the deep layers (IV-VI). CONCLUSIONS: The deep layers of the pre- and parasubiculum appear to control the seizure-induced damage of EC layer III. This phenomenon may be of relevance for epileptogenesis and for the pathogenesis of temporal lobe epilepsy.

Neurons in layer III of the entorhinal cortex. A role in epileptogenesis and epilepsy?

A preferential lesion of neurons in layer III of the entorhinal cortex (EC) is often observed in patients suffering from temporal lobe epilepsy and in several animal models of the disease. This lesion is duplicated in rats by a focal, intra-entorhinal injection of the "indirect" excitotoxin aminooxyacetic acid (AOAA), providing a model that can be used to study the mechanisms underlying seizure-induced cell death and epilepsy. Doomed neurons in the EC and in several associated limbic structures show pathological changes within hours after the AOAA injection, but GABAergic neurons in layer III of the EC are quite resistant. This pattern of neuron loss eventually results in hippocampal and entorhinal hyperexcitability. Notably, the seizure-induced death of layer III neurons in the EC can be attenuated by eliminating the prominent excitatory input from the presubiculum. Taken together, these results suggest opportunities to target parahippocampal structures for the treatment of temporal lobe epilepsy.

A modified technique for tibial interference screw fixation of hamstring anterior cruciate ligament grafts.

This article describes a modified technique for tibial fixation of quadrupled hamstring grafts in anterior cruciate ligament reconstruction. Using this technique common problems with tibial interference screw fixation of hamstring grafts-such as loss of tension of the graft during screw introduction or twisting of the graft in the tunnel around the screw-are avoided.

Ultrastructure and immunocytochemical distribution of GABA in layer III of the rat medial entorhinal cortex following aminooxyacetic acid-induced seizures.

Layer III of the entorhinal cortex (EC) is lesioned in patients with temporal lobe epilepsy (TLE). A similar neuropathology is also present in different animal models of TLE. For example, injection of the "indirect" excitotoxin aminooxyacetic acid (AOAA) into the EC of rats causes behavioral seizures and preferential loss of neurons in layer III of the medial EC. The animals also develop hyperexcitability of the EC and the hippocampal region CA1. To further explore the neuropathological changes within the EC, the ultrastructure and distribution of GABA-like immunoreactivity were assessed in layer III, 28 days after an intraentorhinal AOAA injection. At this time point, light microscopic preparations revealed that a large proportion of pyramidal (putative excitatory) neurons in layer III of the medial EC had degenerated, whereas GABA-immunoreactive neurons had survived. In immunogold-labeled ultrathin sections, the lesioned neuropil was found to contain morphologically intact GABA-containing neurons and nerve terminals. Pathologically swollen dendrites and electron-dense neuronal profiles were present in the lesioned sector as well. The majority of the electron-dense profiles was identified as degenerating dendritic spines that were closely apposed to strongly glutamate-immunopositive axon terminals. Thus, the entorhinal chemoarchitecture is dramatically altered following an episode of AOAA-induced epileptic seizures. One possible consequence of this pathology is a reduced "drive" of the surviving layer III GABA neurons, which in turn may cause hyperexcitability of the EC and the hippocampus. These findings may be of relevance for the genesis and spread of temporal lobe seizures.

Severe heterotopic ossifications after total knee arthroplasty.

The authors report a case of severe heterotopic ossifications after a total knee arthroplasty in an 83-year-old woman. She showed a dramatic loss in range of motion between the third and sixth postoperative week, after she had obtained a satisfactory 0 degree to 90 degrees--range of motion at the 14th postoperative day. A treatment program of radiotherapy combined with indomethacin and nonaggressive antiinflammatory physiotherapy resulted in a slow but steady improvement with complete relief of symptoms 6 months postoperatively.

Glutamate receptor subunits GluR1 and GluR2/3 distribution shows reorganization in the human epileptogenic hippocampus.

The AMPA-type glutamate receptor subunits GluR1 and GluR2/3 were localized by immunohistochemistry with subunit-specific antibodies in hippocampi removed surgically from patients with temporal lobe epilepsy for the control of seizures. The flip and flop splice variants of the subunits were localized by in situ hybridization histochemistry with specific oligoprobes. In patient hippocampi that were not the seizure focus, the GluR1 subunit proteins were diffusely expressed on the dendrites of neurons in all regions. In contrast, in these same hippocampi, the GluR2/3 subunit proteins were expressed strongly on the soma and proximal dendrites of principal neurons in all regions. The flip variant of these subunits was localized in the hilus and fields of Ammon's Horn (CA), while the flop variants were prominent on the dentate granule cells. In the epileptogenic hippocampus, while immunoreactivity was decreased in all fields that showed neuronal loss, there was an increased expression of GluR1 on the dendritic excrescences on the proximal dendrites of hilar neurons and CA3 pyramidal neurons, as well as expression of GluR2/3 in hilar neuron excrescences. Electron microscopic examination confirmed that the GluR1 immunoreactivity was only in dendritic processes, particularly dense at the postsynaptic membranes. Such expression of GluR1 may provide for an enhanced glutamatergic response by these neurons. GluR2/3 was also significantly increased on the dendrites of dentate granule cells in the epileptogenic hippocampus and may provide some protection against excitotoxic injury by reducing calcium flux into neurons.

Neuronal damage after the injection of aminooxyacetic acid into the rat entorhinal cortex: a silver impregnation study.

In rats, most neurons in layer III of the medial entorhinal cortex are exquisitely vulnerable to prolonged seizure activity. These neurons have also been shown to die preferentially in the entorhinal cortex of patients with temporal lobe epilepsy. This lesion can be duplicated in rats by a focal injection of the indirect excitotoxin aminooxyacetic acid into the entorhinal cortex. The present study was designed to examine the neuropathological consequences of an intra-entorhinal aminooxyacetic acid injection at various time-points with a sensitive silver staining method for the visualization of damaged neurons. After 3 h, affected cells with prominently stained processes were readily observed in the transition zone of the hippocampal CA1 field and the subiculum, but no silver-stained neurons were seen in the entorhinal cortex. Less consistently, damaged neurons were observed in the presubiculum, in the temporal and perirhinal cortices and in the lateral amygdaloid nucleus. At 6 h after an aminooxyacetic acid injection, numerous silver-stained neurons, which were typically devoid of processes, were also seen in layer III of the medial entorhinal cortex. This pattern of neurodegeneration remained similar at 12 and 24 h following the aminooxyacetic acid injection, though many silver-stained neurons were noted in layer II of the lateral entorhinal cortex as well. Notably, at five days, silver-stained neurons had disappeared. Instead, dendritic arbors, debris of degenerated neurons and reactive glial cells were present in lesioned brain regions. These data demonstrate the chronology and the extent of neuronal damage following an intra-entorhinal injection of aminooxyacetic acid. The results suggest that a detailed examination of the temporal sequence of neuronal death in the entorhinal cortex and in extra-entorhinal areas is likely to benefit our understanding of the pathophysiology of temporal lobe epilepsy.

Evaluation of Nd:YAG laser membranectomy in blocked tubes after glaucoma tube-shunt surgery.

PURPOSE: To determine the effectiveness of Nd:YAG laser membranectomy for reopening blocked glaucoma tube shunts and maintaining the patency over time. METHODS: We reviewed retrospectively the records of 13 patients (13 eyes) who, during the period January 1990 through June 1996, underwent Nd:YAG laser membranectomy in an attempt to reopen a blocked glaucoma tube shunt. Intraocular pressure and tube patency were evaluated at each follow-up visit. RESULTS: Nd:YAG laser membranectomy effectively opened the blocked glaucoma tube shunts in 11 (84.6%) of 13 eyes. Two tubes could not be reopened. Reblockage occurred in seven eyes (53.8%) within the first 11 weeks; four tubes (30.8%) remained patent through follow-up periods of 39, 82, 106, and 169 weeks. Postlaser complications were moderate anterior chamber reaction in four eyes (30.8%), hyphema in two eyes (15.4%), corneal edema in two eyes (15.4%), pressure spike in one eye (7.7%), and shallow anterior chamber in one eye (7.7%). CONCLUSIONS: Nd:YAG laser membranectomy is effective in reopening blocked glaucoma tube shunts but is associated with a relatively high rate of subsequent reblockage in the initially successful cases.

Quantitative differences between the optic nerve head and peripapillary retina in low-tension and high-tension primary open-angle glaucoma.

PURPOSE: To determine whether quantitative differences in optic nerve topography could be identified between patients having primary open-angle glaucoma with normal intraocular pressure (low-tension primary open-angle glaucoma [LT-POAG]) vs those with elevated intraocular pressure (high-tension primary open-angle glaucoma [HT-POAG]). METHODS: We attempted to match 31 eyes of 31 patients in the LT-POAG group on a case-by-case basis with comparable eyes of 31 patients with HT-POAG. We used the Heidelberg Retina Tomograph to evaluate the optic nerve head and retinal nerve fiber layer. RESULTS: Cup areas and cup:disk area ratios were significantly larger (P < .05), whereas rim areas, rim volumes, retinal nerve fiber layer heights, and retinal nerve fiber layer cross-sectional areas were consistently smaller, but not significantly so (P > .05), in the LT-POAG group. The inferior neuroretinal rim area was significantly smaller (P < .05) and the mean deviation of superior arcuate area was significantly greater than the opposite sector in patients with LT-POAG but not in those with HT-POAG. A relationship between localized measurements of the optic nerve head and mean deviation was more apparent in the LT-POAG group than in the HT-POAG group. CONCLUSIONS: The optic cups were larger in patients with LT-POAG than in those with HT-POAG. Measurements of sectors of the optic disk correlated better with visual field changes in LT-POAG than did global measurements of the whole nerve head, indicating more vulnerability of the optic nerve to focal damage with low intraocular pressure.

Tube-shunt surgery versus neodymium:YAG cyclophotocoagulation in the management of neovascular glaucoma.

OBJECTIVE: To determine the relative effectiveness of neodymium:YAG (Nd:YAG) cyclophotocoagulation (CPC) and tube-shunt surgery on intraocular pressure (IOP) control in eyes with neovascular glaucoma (NVG). DESIGN: Retrospective, case-by-case matched, comparative group study. PARTICIPANTS: Twenty-four patients with NVG treated with noncontact Nd:YAG-CPC were matched with 24 patients who underwent tube-shunt surgery. Matching criteria included the underlying disorder causing angle neovascularization, the lens status, and patient's age. INTERVENTIONS: Tube-shunt surgery or Nd:YAG-CPC. MAIN OUTCOME MEASURE: Postoperative IOP (IOP > or = 6 and < or = 25 mmHg), visual acuity, and presence of any postoperative complications. RESULTS: Satisfactory IOP control (IOP < or = 25 mmHg and > or = 6 mmHg) was achieved in 9 eyes (37.5%) treated with Nd:YAG-CPC compared with 16 eyes (66.7%) receiving a tube-shunt procedure (P = 0.04) over a mean follow-up of 16.9 +/- 14.6 and 15.2 +/- 11.8 months, respectively. In the matched pairs in both groups that had nonequivalent outcomes, the proportions with persistently high IOP or hypotony were both greater in the CPC group than in the tube-shunt group. The cumulative proportion of failure in the CPC group was 20.8% at 6 months, 35.4% at 1 year, and 71.2% at 3 years postoperatively. In the tube-shunt group, the cumulative proportions of failure at 6 months and 1 year were close to those in the CPC group (12.5% and 29.2%, respectively), but lower 3 years after surgery (43.3%). Eleven eyes (45.8%) in the CPC group lost light perception versus four eyes (16.7%) in the tube-shunt group. Complication rate was higher in the tube-shunt group. CONCLUSIONS: This study suggests that, in the management of NVG, tube-shunt surgery more frequently controls IOP in a satisfactory range, with less hypotony and less visual loss, than noncontact Nd:YAG-CPC.

Quantitative estimation of retinal nerve fiber layer height in glaucoma and the relationship with optic nerve head topography and visual field.

PURPOSE: The authors estimated the retinal nerve fiber layer height (RNFLH) measurements in patients with glaucoma compared with those in age-matched healthy subjects as obtained by the laser scanning tomography and assessed the relationship between RNFLH measurements and optic and visual field status. METHODS: Parameters of optic nerve head topography and RNFLH were evaluated in 125 eyes of 21 healthy subjects and 104 patients with glaucoma using the Heidelberg Retina Tomograph ([HRT] Heidelberg Engineering GmbH, Heidelberg, Germany) for the entire disc area and for the superior 70 degrees (50 degrees temporal and 20 degrees nasal to the vertical midline) and inferior 70 degrees sectors of the optic disc. The mean deviation of the visual field, as determined by the Humphrey program 24-2 (Humphrey Instruments, Inc., San Leonardo, CA, U.S.A) was calculated in the entire field and in the superior and inferior Bjerrum area. RESULT: Retinal nerve fiber layer height parameters (mean RNFLH and RNFL cross-sectional area) were decreased significantly in patients with glaucoma compared with healthy individuals. Retinal nerve fiber layer height parameters was correlated strongly with rim volume, rim area, and cup/disc area ratio. Of the various topography measures, retinal nerve fiber layer (RNFL) parameters and cup/disc area ratio showed the strongest correlation with visual field mean deviation in patients with glaucoma. CONCLUSION: Retinal nerve fiber layer height measures were reduced substantially in patients with glaucoma compared with age-matched healthy subjects. Retinal nerve fiber layer height was correlated strongly with topographic optic disc parameters and visual field changes in patients with glaucoma.

Long-term effects of tube-shunt procedures on management of refractory childhood glaucoma.

PURPOSE: The authors evaluated the long-term results of tube-shunt surgery in management of childhood glaucoma. METHODS: The results of tube-shunt surgery in children who had glaucoma refractory to medical or alternative surgical treatment in the Glaucoma Service of Wills Eye Hospital during the period 1986 through 1993 were reviewed. Eighteen eyes of 15 patients were included in the analysis. Follow-up ranged from 14 to 80 months (mean +/- standard deviation, 47.3 +/- 25.1 months). RESULTS: In the early postoperative course (6 months after surgery), the intraocular pressure (IOP) was between 6 and 21 mmHg in 13 eyes (72.2%) with or without glaucoma medication. Two or more years later, IOP was between 6 and 21 mmHg in four eyes without further glaucoma medication (22.2%) and four eyes (22.2%) with the addition of antihypertensive therapy. Five eyes (27.8%) lost light perception, whereas seven (38.9%) remained within one line of preoperative vision or improved. Twelve eyes underwent 28 additional surgical procedures after the tube-shunt operation, mostly to control IOP or manage tube-related complications. CONCLUSION: The limited success rate, relatively high complication rate, and need for frequent surgical intervention suggest caution regarding the prognosis of tube-shunt surgery in children with glaucoma.

Simultaneous monitoring of head-to-cervix forces, intrauterine pressure and cervical dilatation during labour.

In many westernized countries, the caesarean section role has now reached 15% or more, most commonly because of slow progress in labour. In order for labour to result in a vaginal delivery, the uterine cervix must dilate to allow the foetus to travel through the birth canal. This process is driven by uterine contractions, but the mechanisms by which the contractions result in cervical dilatation are still far from clear. The force exerted by the presenting part (foetal head) on the cervical tissue during contractions (head-to-cervix force, HCF) has been shown to be the variable with the best correlation with cervical dilatation. Unfortunately, the mechanism by which these two variables are related is still poorly understood. In order to investigate the relationship between head-to-cervix force, intrauterine pressure (IUP) and cervical dilatation, we have developed a system for their simultaneous and continuous monitoring during labour. The HCF is measured by using a novel intrauterine probe which is slipped alongside the foetal head so as to lie sandwiched between the latter and the cervix. The probe is fitted with six specially designed miniature force sensors, spaced 1.8 cm apart, which respond linearly and approximate the behaviour of load cells. They are interfaced with a PC by circuitry that allows auto-zeroing and drift compensation. The system enables simultaneous acquisition of intrauterine pressure and foetal heart rate (measured using a Sonicaid Meridian foetal monitor) via a serial link, together with continuous cervical dilatation measured by a caliper-like device applied to the cervix. Some preliminary data are presented, which suggest that the system can be used to investigate the role played by head-to-cervix force and intrauterine pressure in the cervix dilatation process.