Chronic migraine associated with the Chiari type 1 malformation

Kaplan, Yüksel; Öksüz, Erol

doi:10.1016/j.clineuro.2008.05.016

Cited by 24 publications

(18 citation statements)

References 11 publications

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“…Sleep apnea, neck pain, and feeding problems are more frequent in young children [2] while headache and neurological deficits are more peculiar of older children, adolescents, and adults [32]. In spite of these differences in the presentation, the clinical picture is chronically developing and slowly progressing in the large majority of CI patients [23,27,43]. Acute onset is actually thought to be rare and often related to the coexistence of syringomyelia [42,45].…”

Section: Discussionmentioning

confidence: 99%

Abrupt clinical onset of Chiari type I/syringomyelia complex: clinical and physiopathological implications

et al. 2012

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Chiari I malformation (CI) continues to raise great interest among physicians due to the larger and larger number of newly diagnosed cases. The clinical and radiological picture and the management options of such a chronic disease are well acknowledged as well as those of the associated syringomyelia. Little is known, on the other hand, about abrupt clinical onset following decompensation of CI/syringomyelia complex. This review on the sudden onset of these two conditions shows that this is a very rare phenomenon; only 41 cases are being reported in the last three decades. In all these cases, acute onset was referable to CI/syringomyelia and the clinical course quickly precipitated. Motor deficits (36.5 %), respiratory failure (29 %), cranial nerve palsy (17 %), and cardiac arrest (14.5 %) were the most common findings, thus confirming that abrupt onset may have severe and life-threatening consequences. Indeed, sudden or early mortality accounted for 19.5 % of cases. In spite of that, most of the surviving subjects had an excellent outcome following either surgical or medical/rehabilitation treatment. Physiopathology of abrupt onset is attributed to the acute compression of the brainstem/upper cervical spinal cord by ectopic tonsils and syringobulbia/syringomyelia, frequently precipitated by a minor injury, followed by impairment of medullary baroreceptors and midbrain reticular substance (cardiac arrest, syncope), medullary chemoreceptors and phrenic nerve nuclei (respiratory failure), lower cranial nerve nuclei (cardiac arrest, cranial nerve palsy), and pyramidal tracts (motor deficits). About 87 % of patients of this review were asymptomatic prior to their acute onset. The problem of the management of asymptomatic subjects is still open.

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Section: Discussionmentioning

confidence: 99%

Abrupt clinical onset of Chiari type I/syringomyelia complex: clinical and physiopathological implications

et al. 2012

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“…Migraine headaches associated with abnormal cerebellar anatomy (e.g., Chiari malformation) and function (e.g., dizziness, ataxia, poor motor coordination) are well documented (Kaplan and Oksuz, 2008; Russell and Ducros, 2011; Vincent and Hadjikhani, 2007), and convincingly evident by imaging studies that show multiple subclinical cerebellar infarct-like lesions in migraine aura patients (Kruit et al, 2004; Kruit et al, 2005; Kruit et al, 2010; Scher et al, 2009). In fact, cerebellar abnormalities in migraine have been elegantly demonstrated in translational genetic studies on familial hemiplegic migraine as well (Ferrari et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Brain network alterations in the inflammatory soup animal model of migraine

et al. 2017

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Advances in our understanding of the human pain experience have shifted much of the focus of pain research from the periphery to the brain. Current hypotheses suggest that the progression of migraine depends on abnormal functioning of neurons in multiple brain regions. Accordingly, we sought to capture functional brain changes induced by the application of an inflammatory cocktail known as inflammatory soup (IS), to the dura mater across multiple brain networks. Specifically, we aimed to determine whether IS alters additional neural networks indirectly related to the primary nociceptive pathways via the spinal cord to the thalamus and cortex. IS comprises an acidic combination of bradykinin, serotonin, histamine and prostaglandin PGE2 and was introduced to basic pain research as a tool to activate and sensitize peripheral nociceptors when studying pathological pain conditions associated with allodynia and hyperalgesia. Using this model of intracranial pain, we found that dural application of IS in awake, fully conscious, rats enhanced thalamic, hypothalamic, hippocampal and somatosensory cortex responses to mechanical stimulation of the face (compared to sham synthetic interstitial fluid administration). Furthermore, resting state MRI data revealed altered functional connectivity in a number of networks previously identified in clinical chronic pain populations. These included the default mode, sensorimotor, interoceptive (Salience) and autonomic networks. The findings suggest that activation and sensitization of meningeal nociceptors by IS can enhance the extent to which the brain processes nociceptive signaling, define new level of modulation of affective and cognitive responses to pain; set new tone for hypothalamic regulation of autonomic outflow to the cranium; and change cerebellar functions.

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“…In this disorder, the cerebellar tonsils (the lower part of the cerebellum) extend into the foramen magnum (the hole in the base of the skull through which the spinal cord passes) without involving the brainstem (Novegno et al, 2008). Symptoms are not always present, but common manifestations of ACM can include chronic migraine headaches (Kaplan & Oksuz, 2008); numbness in arms or legs; dizziness difficulty swallowing; vomiting; ringing/buzzing in the ears; insomnia; sleep apnea; and depression (National Institute of Neurological Disorders and Stroke [NINDS], 2009;Novegno et.al., 2008). The lower cranial nerves can also be affected (Rosenbaum & Ciaverella, 2004), potentially causing dysfunction in facial muscles, hearing, balance, tongue movement, sense of taste, trapezius muscles (shoulder shrug), and/or pharynx (gag reflex).…”

Section: Medical Historymentioning

confidence: 98%

“I Fired My Last Doctor for Not Taking Me Seriously”: Collaborating With a Difficult Medical Patient in a Multidisciplinary Primary Care Facility

Skillings

Murdoch

Porcerelli

2010

Journal of Personality Assessment

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We present the case of a multidisciplinary primary care assessment of a 32-year-old woman with multiple medical and psychological complaints. Following the collaborative care model, this assessment was conducted by a team consisting of a clinical health psychologist, Dr. J. L. Skillings, and a family physician, Dr. W. J. Murdoch. We describe the primary care environment in which this referral was made including the methods that were utilized to insure a successful professional collaboration. We report the results and recommendations from a comprehensive biopsychosocial assessment; we place emphasis on the psychological diagnosis and pain symptoms. We also describe the feedback session in which the assessment results were provided to the patient and her spouse by both physician and psychologist. Multiperspective commentary about the assessment is offered by the patient and her husband as well as the physician and psychologist assessors.

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Chronic migraine associated with the Chiari type 1 malformation

Cited by 24 publications

References 11 publications

Abrupt clinical onset of Chiari type I/syringomyelia complex: clinical and physiopathological implications

Abrupt clinical onset of Chiari type I/syringomyelia complex: clinical and physiopathological implications

Brain network alterations in the inflammatory soup animal model of migraine

“I Fired My Last Doctor for Not Taking Me Seriously”: Collaborating With a Difficult Medical Patient in a Multidisciplinary Primary Care Facility

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