HPV-positive clinically advanced squamous cell carcinoma of the urinary bladder (aBSCC): A comprehensive genomic profiling (CGP) study.

BACKGROUND: Advanced bladder squamous cell carcinoma (aBSCC) is an uncommon form of urinary bladder malignancy when compared with the much higher urothelial carcinoma incidence. We studied the genomic alteration (GA) landscape in a series of aBSCC based on the association with human papilloma virus (HPV) to determine if differences in GA would be observed between the positive and negative groups. METHODS: Using a hybrid capture-based FDA-approved CGP assay, a series of 171 aBSCC were sequenced to evaluate all classes of GA. Tumor mutational burden (TMB) was determined on up to 1.1 Mbp of sequenced DNA and microsatellite instability (MSI) was determined on up to 114 loci. Programmed cell death ligand -1 (PD-L1) expression was determined by IHC (Dako 22C3) with negative expression when PD-L1 was 0, lower expression of positivity set at 1 to 49%, and higher expression set at ≥50% expression. RESULTS: Overall, 11 (6.4%) of the aBSCC were found to harbor HPV sequences (10 HPV16 and 1 HPV 11). HPV+ status was identified slightly more often in women (NS) and in younger patients (P = 0.04); 2 female patients with aBSCC had a prior history of SCC including 1 anal SCC and 1 vaginal SCC. HPV+ aBSCC had fewer GA/tumor (P < 0.0001), more inactivating mutations in RB1 (P = 0.032), and fewer inactivating GA in CDKN2A (P < 0.0001), CDKN2B (P = 0.05), TERT promoter (P = 0.0004) and TP53 (P < 0.0001). GA in genes associated with urothelial carcinoma including FGFR2 and FGFR3 were similar in both HPV+ and HPV- aBSCC groups. MTAP loss (homozygous deletion) which has emerged as a biomarker for PRMT5 inhibitor-based clinical trials was not identified in any of the 11 HPV+ aBSCC cases, which was significantly lower than the 28% positive frequency of MTAP loss in the HPV- aBSCC group (P < 0.0001). MTOR and PIK3CA pathway GA were not significantly different in the 2 groups. Putative biomarkers associated with immunotherapy (IO) response, including MSI and TMB status, were also similar in the 2 groups. PD-L1 expression data was available for a subset of both HPV+ and HPV- cases and showed high frequencies of positive staining which was not different in the 2 groups. CONCLUSIONS: HPV+ aBSCC tends to occur more often in younger patients. As reported in other HPV-associated squamous cell carcinomas, HPV+ aBSCC demonstrates significantly reduced frequencies of inactivating mutations in cell cycle regulatory genes with similar GA in MTOR and PIK3CA pathways. The implication of HPV in the pathogenesis of bladder cancer remains unknown but warrants further exploration and clinical validation.

Alteration of pain recognition in schizophrenia.

BACKGROUND: Schizophrenia patients display impaired recognition of their own emotions and those of others and deficits in several domains of empathy. The first-person experience of pain and observing others in pain normally trigger strong emotional mechanisms. We therefore hypothesized that schizophrenia patients would display impaired recognition and categorization of both their own pain and the pain of others. METHODS: We studied 29 patients (18 men/11 women; 36 ± 13 years old) with paranoid schizophrenia-spectrum disorder and 27 healthy volunteers (20 men/7 women; 31 ± 9 years old) matched for age, gender, IQ and socio-cultural level. We assessed symptom severity and theory of mind. The participants' ability to detect and categorize pain in others was assessed with the sensitivity to expressions of pain (STEP) test, which is based on facial expressions, and another dynamic test involving a series of video sequences showing various pain-inducing events. The ability of patients to evaluate their own pain was assessed with the situational pain questionnaire (SPQ), which includes a series of questions assessing how one would expect to feel in different imaginary situations. Empathic tendencies were assessed with the interpersonal reactivity index. RESULTS: Patients and controls differed significantly in STEP, pain video and SPQ scores. By contrast with control subjects, the patients' pain judgements were not correlated with their affective or cognitive empathic capacities. CONCLUSIONS: Schizophrenic patients have a deficit of the identification and categorization of pain both in themselves and in others.

[Congenital insensitivity to pain]. / L'insensibilité congénitale à la douleur.

Congenital insensitivity to pain (CIP) is a rare syndrome with various clinical expressions, characterized by a dramatic impairment of pain perception since birth. In the 1980s, progress in nerve histopathology allowed to demonstrate that CIP was almost always a manifestation of hereditary sensory and autonomic neuropathies (HSAN) involving the small-calibre (A-delta and C) nerve fibres which normally transmit nociceptive inputs along sensory nerves. Identification of the genetic basis of several clinical subtypes has led to a better understanding of the mechanisms involved, emphasizing in particular the crucial role of nerve growth factor (NGF) in the development and survival of nociceptors. Recently, mutations of the gene coding for the sodium channel Nav1.7--a voltage-dependent sodium channel expressed preferentially on peripheral nociceptors and sympathetic ganglia--have been found to be the cause of CIP in patients showing a normal nerve biopsy. This radical impairment of nociception mirrors the hereditary pain syndromes associated with "gain of function" mutations of the same ion channel, such as familial erythromelalgia and paroxysmal extreme pain disorder. Future research with CIP patients may identify other proteins specifically involved in nociception, which might represent potential targets for chronic pain treatment. Moreover, this rare clinical syndrome offers the opportunity to address interesting neuropsychological issues, such as the role of pain experience in the construction of body image and in the empathic representation of others' pain.

[Pathophysiology of pain in venous disease]. / Physiopathologie de la douleur au cours de la maladie veineuse.

Pain is the leading complaint of patients with venous disease. It has a significant effect on the patient's quality-of-life. For the clinician and the researcher however it is difficult to apprehend how pain is related to the venous disease, both because of the multiple factors involved and because of the lack of any strong relationship between pain symptoms and the severity of the venous disease. Currently, several hypotheses concerning the pathogenesis of pain in venous disease have focused on the causal impact of local inflammation. Over the last five years, a large body of evidence has been accumulation showing an inflammatory reaction around varicose veins, but the precise mechanism of how inflammatory mediators interact with venous nociceptors, which might explain part of the variability in pain observed in venous disease, remains elusive, both clinically and experimentally.

[Neurological basis of the emotional dimension of pain]. / Bases neurologiques de l'affect douloureux.

Feeling pain is in the same time a sensory and an affective experience. Pain asymbolia and prefrontal lobotomy, two distinct neurological pictures, help to better understand the cerebral basis of the emotional dimension of pain. In pain asymbolia, the selective alteration of the affective dimension of pain is associated with a loss of the sense of threat and danger. Following prefrontal lobotomy, the emotional impact of chronic pain is dramatically reduced, while affective responses to acute pain are paradoxically increased. Such clinical observations allow to make a clear distinction between immediate pain unpleasantness on the one hand, and secondary pain affect, linked to the significance of the pain experience in terms of the self and of the future, on the other hand. Moreover, recent functional neuroimaging data allow to better define the neural substrates of the affective dimension of pain and to highlight the shared neuro-anatomical networks between physical and psychic suffering.

Tension-type headache as the unique pain experience of a patient with congenital insensitivity to pain.

Congenital insensitivity to pain (CIP) is a rare clinical syndrome characterized by dramatic impairment of pain perception since birth and is generally caused by a hereditary sensory and autonomic neuropathy (HSAN) with loss of the small-calibre, nociceptive nerve fibres. We report the case of a 32-year-old woman with CIP and a presumptive diagnosis of HSAN type V, who experienced physical pain for the first and unique time in her life shortly after the sudden loss of her brother. This patient had sustained innumerable painless injuries during childhood, including bone fractures and severe burns. The only pain she ever felt consisted in an intense headache, which took place in a context of strong emotional overload and anxiety, 3 weeks after her younger brother died suddenly in a car accident. The description of this inaugural episode of headache fulfilled the diagnostic criteria of episodic tension-type headache. This case strongly suggests that the transcription of the grief of bereavement into physical pain may sometimes occur independently of the peripheral mechanisms of nociception and despite the lack of previous pain experience. In the light of recent experimental data showing that the same neural mechanisms that regulate physical pain may also control the expression of separation distress and the feeling of social exclusion, this unique case helps to better understand why some patients may feel physically hurt after the loss of someone they love.

The phenomenology of body image distortions induced by regional anaesthesia.

Patients with peripheral nerve or spinal cord lesions frequently report perceptual distortions related to position, shape, texture or temperature of the affected areas. This study aimed to describe the phenomenology of such body image alterations during the course of upper limb, lower limb or spinal anaesthetic blocks in patients (n = 36) undergoing orthopaedic surgery. Multimodal sensory testing and assessment of motor function were performed at regular intervals, and the relationship between the reported body image distortions and the progression of sensory and motor impairment was analysed. We found that perceptual changes concerning the shape and size of the deafferented limb occurred in the great majority of patients. In all of them, illusions of swelling, elongation or shortening of the limb coincided with the impairment of warm, cold and/or pinprick sensations, suggesting that thin myelinated Adelta- and/or unmyelinated C-fibres may provide a source of tonic modulation to the limb's cortical representation. Such perceptual alterations of shape and size of body parts differed clearly from postural illusions in terms of frequency, time course and influence of vision. In addition to perceptual changes in the deafferented area, almost half of the patients felt their unanaesthetized lips and/or mouth swelling during the course of upper limb block, suggesting the unmasking of dynamic interactions between somatotopically adjacent cortical representations. Conflicting sensations could co-exist in the patient's body image, such as the illusion of swelling of a limb, which, at the same time, was felt to be missing. The sense of ownership of the deafferented limb was impaired in some cases. These observations show that the perception of body shape and the awareness of its postural variations are built from different plastic models. They also underline the contribution of peripheral afferent activity to the maintenance of a unified body image.

Stage-dependent changes in the modulation of spinal nociceptive neuronal activity during the course of inflammation.

Spinal and supraspinal controls can tonically or phasically modulate the output of spinal nociceptive neurons. Alterations of these modulatory systems have been described during the acute stage of inflammation. In the present study in the rat, tonic descending controls were assessed during acute (24--48 h) and chronic (3--4 weeks) stages of monoarthritis of the ankle. The electrophysiological properties of spinal convergent neurons with ankle input were compared before and after spinalization. In a parallel series of experiments, spinal convergent neurons were recorded from the normal side in order to assess the propriospinal and supraspinal inhibitory controls triggered by nociceptive stimulation of the inflamed ankle. Tonic descending inhibition of convergent neurons with input from the inflamed ankle was enhanced during the acute stage and then decreased during the chronic stage of monoarthritis. Contralateral-induced inhibitions exhibited a similar temporal evolution. Time-dependent changes in the spinal transmission of nociceptive signals were shown by removing descending modulation in animals with monoarthritis; sensitization of spinal neurons with input from the inflamed ankle was demonstrated during the acute stage of monoarthritis, whereas a crossed transmission between inflamed and normal sides was observed during the chronic stage of the disease. These results show that dynamic and stage-dependent modifications of descending controls tend to dampen the central changes associated with inflammation.

Further evidence for a central reorganisation of synaptic connectivity in patients with hypoglossal-facial anastomosis in man.

In normal subjects, electrical stimulation of trigeminal mucosal afferents (lingual nerve - V3) can elicit a short latency (12.5+/-0. 3 ms; mean+/-S.D.) reflex response in the ipsilateral genioglossus muscle (Maisonobe et al., Reflexes elicited from cutaneous and mucosal trigeminal afferents in normal human subjects. Brain Res. 1998;810:220-228). In the present study on patients with hypoglossal-facial (XII-VII) nerve anastomoses, we were able to record similar R1-type blink reflex responses in the orbicularis oculi muscles, following stimulation of either supraorbital nerve (V1) or lingual nerve (V3) afferents. However, these responses were not present in normal control subjects. Voluntary swallowing movements produced clear-cut facilitations of the R1 blink reflex response elicited by stimulation of V1 afferents. In a conditioning-test procedure with a variable inter-stimulus interval, the R1 blink reflex response elicited by supraorbital nerve stimulation was facilitated by an ipsilateral mucosal conditioning stimulus in the V3 region. This facilitatory effect was maximal when the two stimuli (conditioning and test) were applied simultaneously. This effect was not observed on the R1 component of the blink reflex in the normal control subjects. These data strongly suggest that in patients with XII-VII anastomoses, but not in normal subjects, both cutaneous (V1) and mucosal (V3) trigeminal afferents project onto the same interneurones in the trigeminal principal sensory nucleus. This clearly supports the idea that peripheral manipulation of the VIIth and the XIIth nerves induces a plastic change within this nucleus.

Alteration of descending modulation of nociception during the course of monoarthritis in the rat.

Diffuse noxious inhibitory controls (DNIC), which involve supraspinal structures and modulate the transmission of nociceptive signals, were investigated at different stages during the development of adjuvant-induced monoarthritis in the rat. After behavioral evaluation, recordings of trigeminal convergent neurons were performed in anesthetized animals with acute (24-48 hr) or chronic (3-4 weeks) monoarthritis of the ankle. Inhibitions of C-fiber-evoked neuronal responses during and after the application of noxious conditioning stimuli to the ankle were measured to evaluate DNIC. The conditioning stimuli consisted of mechanical (maximal flexion and graded pressures) and graded thermal stimuli and were applied alternately to normal and arthritic ankles. Behaviorally, the two groups of animals exhibited a similar increased sensitivity to mechanical stimuli applied to the arthritic joint (i.e., an increased ankle-bend score and a decreased vocalization threshold to pressure stimuli). However, they showed different electrophysiological profiles. In the animals with acute monoarthritis, the DNIC-induced inhibitions produced by mechanical or thermal stimulation of the arthritic joint were significantly increased at all intensities compared with the normal joint. In contrast, in the chronic stage of monoarthritis, the DNIC-induced inhibitions triggered by thermal or pressure stimuli were similar for both ankles, except with the most intense mechanical stimuli. This discrepancy between the behavioral and electrophysiological findings suggests that inputs activated during chronic monoarthritis may fail to recruit DNIC and may thus be functionally different from those activated in the acute stage of inflammation.

Depressive effects of segmental and heterotopic application of transcutaneous electrical nerve stimulation and piezo-electric current on lower limb nociceptive flexion reflex in human subjects.

OBJECTIVES: To evaluate quantitatively the effectiveness and clinical relevance of various parameters of electrical stimulation used to relieve acute and chronic pain and to further knowledge of the mechanisms that may underlie the physiologic response produced by the transcutaneous application of each type of current. DESIGN: A nociceptive flexion reflex (RIII reflex) elicited in the lower limb by electrical stimulation of the sural nerve at the ankle was studied before, during, and after application of the following conditioning stimuli: (1) non-noxious transcutaneous electrical nerve stimulation (TENS)--low-intensity (2mA), short-duration (0.1 msec), and high-frequency (100Hz) rectangular pulses (TENS1); (2) noxious TENS--high-intensity (20mA), long-duration (2 msec), and low-frequency (3Hz) rectangular pulses (TENS2); (3) noxious piezo-electric current (PEC)--high-voltage, low-charge, low-intensity, and low-frequency rectangular pulses delivered by a piezo-electric ceramic device (PECs1); (4) a sham PEC situation in which the piezo-electric device did not produce any electric current (Sham PEC). Each conditioning stimulus (TENS1, TENS2, PECs1, Sham PEC) was applied for a 2-minute period either segmentally on the sural nerve itself or heterotopically on the skin overlying the first interosseous space of the contralateral hand. PARTICIPANTS: Twenty-four healthy volunteers (14 women, 10 men, 19 to 52 years of age), who were briefed and familiarized with the experimental procedure. During the experimental sessions, subjects were prone in bed to ensure muscular relaxation. MEASURES: Value of the nociceptive RIII reflex before, during, and after application of conditioning stimuli in the four procedures described above. This reflex was selected because it has been shown to be an objective and physiologic correlate of pain. RESULTS: Non-noxious TENS1 stimulation applied segmentally produced inhibitions of the RIII reflex only during the 2-minute conditioning period. When given segmentally, the noxious TENS2 stimulation produced a facilitatory effect during the 2 minutes of application, followed by significant inhibitory after-effects. The administration of TENS2 heterotopically resulted in inhibitions of the RIII reflex both during and after the 2-minute conditioning period. Application of PECs1, whether segmentally or heterotopically, produced powerful and long-lasting inhibitory after-effects, especially with the heterotopic paradigm. These effects were associated with long-lasting local changes to the skin of the neurogenic inflammation type, which were well tolerated by all subjects. Application of Sham PEC did not result in significant modification of either the RIII reflex or the skin. CONCLUSIONS: These data are discussed in terms of possible spinal and supraspinal mechanisms involving inhibitory descending controls and underline the potential clinical use of PECs1 in the treatment of pain.

[Visual hallucinosis and hyperhedonism in pontine and thalamic infarction]. / Hallucinose visuelle et hyperhédonisme au cours d'un infarctus pontique et thalamique.

The syndrome of peduncular hallucinosis in characterized by transient visual hallucinations which often consist in animated and mobile characters or animals, and which are often associated with disordered sleep. Although vivid and life) like, these hallucinations are generally not mistaken for reality. In view of the associated neurological symptoms, this syndrome was first believed to occur only with lesions of the mesencephalon. Lesions restricted to the mesencephalon have been identified with MRI in a few cases and were demonstrated by pathological verification in one patient with this syndrome. We describe a patient who experienced very similar hallucinations following a unilateral infarct restricted to the cerebellum, rostral protuberance and posterior thalamus. No lesion was seen in the mesencephalon with MRI. This case confirms that the lesions responsible for peduncular hallucinosis are not restricted to the mesencephalon, which suggests that several interconnected neural structures are probably involved in the genesis of this type of visual hallucinations. During the days following the stroke, our patient also experienced transient sensations of pleasure which he considered as abnormal. In view of the site of the lesions in this case, the visual hallucinations may be explained by a disinhibition of ponto-geniculo-occipital waves. A transient activation of reward-system pathways traveling in the brainstem ventral tegmentum may have contributed to the occurrence of the abnormal sensations of pleasure.

A clinical and neurophysiological study of a patient with an extensive transection of the spinal cord sparing only a part of one anterolateral quadrant.

In 1976, Noordenbos and Wall studied sensory functions in a woman with a surgically verified T3 spinal cord transection which spared only a part of the left anterolateral quadrant, We re-investigated this unique case 18 years after the lesion and included a comparable sensory examination, MRI of the spinal cord, somatosensory evoked potentials, PET-activation study during hand and foot vibration and analysis of flexion reflex modulation during the Jendrassik manoeuvre. Our results show that the residual anterolateral quadrant contains ascending pathways carrying a wide range of sensory information as well as descending pathways modulating flexion reflex activity at the spinal level. Moreover, the changes in sensory functions and the unique pattern of cortical activation suggest a functional reorganization of the connectivity between the periphery and the cerebral cortex. Changes of facilitation and/or of inhibition at different levels of the somatosensory system may account for these longterm plastic changes.

Cellular expression, developmental regulation, and phylogenic conservation of PEA-15, the astrocytic major phosphoprotein and protein kinase C substrate.

PEA-15 has recently been identified as a major phosphoprotein in astrocytes and an endogenous substrate for protein kinase C. This 15-kDa protein exists under three molecular forms, an unphosphorylated form, N, and two phosphorylated forms, Pa and Pb. Antisera were raised against synthetic peptides corresponding to the internal sequences of the mouse protein containing the two specific phosphorylation sites and affinity-purified antibodies were used for immunoblotting. PEA-15 was found mainly in the cytosol, but its protein kinase C-phosphorylated form, Pb, was also detectable in association with the membrane and remained with the fraction that contains stabilized microtubules. Abundant in astrocytes, particularly in the hippocampus, PEA-15 was also detected in all cultured brain cell types examined, indicating a more ubiquitous distribution of the protein, further demonstrated by its detection in the eye and in the lung. Parallel to the increase in expression levels, phosphorylation of PEA-15 also increased during development. This paralleled results obtained in primary cultures, whereas PEA-15 levels increase with cell maturation. Finally, physiological importance of PEA-15 phosphorylation was illustrated by immunoreactivity observed in brain homogenates of different mammals, birds, amphibians, and fish.

Partial restoration of blink reflex function after spinal accessory-facial nerve anastomosis.

Functional motor control requires perfect matching of the central connections of motoneurons with their peripheral inputs. It is not known, however, to what extent these central circuits are influenced by target muscles, either during development or after a lesion. Surgical interventions aimed at restoring function after peripheral nerve lesions provide an opportunity for studying this interaction in the mature human nervous system. A patient was studied in whom the spinal accessory nerve was anastomosed into a lesioned facial nerve, allowing voluntary contractions of the previously paralysed muscles. This procedure, in addition to replacing the facial neurons at peripheral synapses, allowed a new short latency trigeminospinal accessory reflex of the R1 blink reflex type to be demonstrated, implying that trigeminal neurons had sprouted towards spinal accessory motoneurons over a distance of at least 1 cm. These results show an unexpected influence of the periphery in remodelling central connectivity in humans. The motoneuronal excitability for this R1 reflex response was therefore studied to compare the convergent properties of facial motoneurons (normal side) with those of the spinal accessory motoneurons (operated side) using a classic double shock technique with variable interstimulus intervals (conditioning test stimulus). On the normal side, conditioning stimuli (to the ipsilateral or contralateral infraliminar supraorbital nerve) produced a clearcut facilitation of the R1 blink reflex when the interstimulus interval was 30-80 ms. By contrast, a similar procedure had no effect on the R1 blink reflex mediated via the trigeminal-spinal accessory reflex arc. These data indicate that despite the heterotopic sprouting of some axons from neurons in the XIth nucleus, motoneurons involved in the newly formed reflex arc remain totally inexcitable by other trigeminal afferents and seem unable to ensure a physiological functioning of the normal blink reflex. Thus the functional relevance of the recovered R1 blink response remains unclear.

[Unilateral paralysis of the lower cranial nerves caused by lesion of the internal carotid artery]. / Paralysie unilatérale des derniers nerfs crâniens par lésion de l'artère carotide interne.

We report two cases of unilateral, isolated lower cranial nerves (IX, X, XI and XII) palsy: both were due to a lesion of the internal carotid artery in the para-pharyngeal space (a dissection and a pseudoaneurysm). The diagnosis was based upon magnetic resonance imaging and selective angiography. The normality of the external carotid artery on angiography led to the hypothesis of a direct compression of the lower cranial nerves in the para-pharyngeal space, rather than an ischemia of these nerves.

Characterization of PEA-15, a major substrate for protein kinase C in astrocytes.

Astrocytes in the central nervous system are involved in a variety of functions including storage of glycogen, maintenance of the extracellular ionic equilibrium, and support for the migration and the differentiation of neurons. Astrocytes express membrane receptors allowing them to respond to extracellular signals. Activation of receptors induces a cascade of events, such as stimulation of protein kinases and subsequent phosphorylation of target proteins. To understand the regulatory processes underlying neuroglial interactions, attempts were made to identify major phosphorylated proteins in striatal astrocytes, grown in primary culture and labeled with [32P]phosphate. Two-dimensional gel electrophoresis revealed a major doublet, Pa and Pb, of highly labeled spots, with a low molecular weight (M(r) = 15,000) and acidic pI (pI = 5.2 and 5.3, respectively). Using an enriched, heat-stable, cytosolic fraction, Pa and Pb were eluted from semi-preparative two-dimensional gels and subjected to a limited proteolysis and partial microsequencing. The same sequences were obtained within Pa and Pb and had no homology with other known protein. Antibodies raised against corresponding synthetic peptides confirm that the doublet represents two isoelectric variants of the same protein, which also exists under a nonphosphorylated form, N. We propose to name this protein PEA-15, for Phosphoprotein Enriched in Astrocytes-15 kDa, according to its large enrichment in these cells. Treatment of intact astrocytes with 12-O-tetradecanoylphorbol-13-acetate (TPA), which stimulates protein kinase C (PKC), increased the phosphorylation of the more acidic spot (Pb) while decreasing Pa intensity. Stimulations of astrocytes known to increase PKC activity, i.e. noradrenaline, or its inhibition by decreasing extracellular calcium concentrations, staurosporine, or desensitization following long term treatment with TPA, induced a phosphorylation or a dephosphorylation of PEA-15, respectively. Using purified PKC, PEA-15 appeared to be a good substrate in vitro. Two-dimensional peptide mapping revealed that the phosphorylation site in intact cells was identical with the site phosphorylated by PKC in vitro. Mapping the phosphopeptides by HPLC following endolysine C treatment lead to the identification of a sequence, phosphorylated in intact astrocytes and in vitro by PKC, containing a consensus site for PKC: LTRIPSAKK. Antibodies raised against a synthetic peptide derived from this sequence recognized N and Pa in control conditions and Pb after its dephosphorylation. Thus, PEA-15 is an endogenous substrate for PKC, the kinase mediating the transition from Pa to Pb.

[Arachnoid cyst of the temporal fossa. Subdural hematoma. Contribution of MRI]. / Kyste arachnoïdien de la fosse temporale. Hématome sous-dural. Apport de l'IRM.

A 20-year old man presented with an arachnoid cyst of the middle fossa and a subdural hematoma (SDH). An intra-cystic hemorrhage masked the presence of the SDH on CT. MRI demonstrated a communication between cyst and SDH. The mechanism of SDH formation is discussed.