Differentiating Headaches ,testing and Management Dr Bhadresh B Mangukiya D.M.Neurology (Clinic-504,Param doc House,Station road ,surat)

Talk………………….. Basic stuctures and pathophysiology Primary or secondary headache? Differ primary Headache? What is natural History disease? EEG ,MRI ,CT SCAN and OTHERS Role When to start prophylaxis? Drug of Choice?

Pain-sensitive structures in the head and neck Extra-cranial Scalp Scalp muscles Skull Carotid and vertebral arteries Paranasal sinuses Eyes and orbits Mouth, teeth, and pharynx Ears Cervical spine and ligaments Cervical muscles Intracranial Periosteum Cranial nerves Meninges Meningeal arteries and dural sinuses Proximal intracranial arteries Sphenoid sinus Thalamic nuclei Brainstem pain-modulating centers

What causes Hedache?

What are common causes?

Differential diagnosis of 906 patients who presented to a general neurology clinic with headache or facial pain as the major or only symptom Diagnosis Number % Tension headache 296 32 Migraine 241 27 Headache ? Cause 139 15 Post-traumatic 71 8 Facial pain ?cause 38 4 Depression 29 3 Trigeminal neuralgia 29 3 Cluster headache 19 2 Malignant IC Tumour 14 1.5 Benign IC Tumour 9 Temporal arteritis 6 Post-herpetic neuralgia 5 Benign IC hypertension 4 Cough headache 3 Subdural haematoma 2 Sinus infection 1

Headache Diagnosis and Testing

RED FLAGS SITUATION DIFFERRENTIAL WORK UP Age > 50 Yrs Temporal Artritis, SOL ESR, Imaging Age < 20 Yrs Sudden Onset SAH, Pitutary Apoplexy, Mass Lesion, Hemorrhage into a mass lesion, Aneurysm Rupture. Neuroimaging, L.P Increasing in Frequency & Severity Subdural Hematoma, SOL, Med Over Use Neuroimaging, Med Screening New Onset Headache in a Pt with Risk Factors ie HIV, Cancer Meningitis, Brain Abscess, Metastases “” Headache with Sign of Systemic Illness Fever, Neck Rigidity Meningitis, Encephalitis, Lyme Disease, Collagen Vascular Disease, Systemic Infection Serology Focal Neurological Signs SOL, Stroke, Infarction, Collagen Vascular Disease Neuroimaging, Collagenvascular evaluation Incl Antiphospholipid antibodies. Papilledema SOL, BIH, Meningitis Subsequent to Trauma IC Hemorrhage, Sub/Epi dural Hematoma,Post Trauma Headache Neuroimaging of Skull, Brain & C Spine

Investigations FBC & ESR. X-Ray Skull, Paranasal Sinuses, Cervical Spine. CT Scan of the head. MRI of the Brain. Eye & ENT Evaluation. Cardiologic & Renal Evaluation.

Autonomi c Cephalgias

Migraine Terminology migraineurs: person who experiences migraines aura: collection of symptoms that may precede or co-occur; typically visual, lasts less than 1 hour positive features scintillations: a rapidly oscillating pattern of visual distortions photopsia: perception of flashes of light teichopsia: spot of flickering light negative features scotoma: an area of diminished vision within the visual field hemianopsia: blindness in half of the visual field, may involve one or both eyes hemiplegic aura: occurring on one side of body basilar type aura: aura is localized to the brainstem DiPiro et al. (2008). Pharmacotherapy: A Pathophysiologic Approach. p. 1008.

Release of Neurotransmitters Presymptomatic hyperexcitabilty increases brain stem response to triggers Release of Neurotransmitters (5-HT, NE, DA, GABA, Glutamate, NO, CGRP, Substance P, Estrogen) Neurotransmitters activate the Trigeminal Nucleus Dilation of Meningeal blood vessels (Throbbing) Activation of Area Postrema (N/V) Activation of Hypothalamus (Hypersensitivity) Activation of cervical trigeminal system (Muscle spasm) Triggers = certain foods, skipping meals, poor sleep, stress, smells, barometric pressure changes Most medications for acute treatment and migraine prevention work on one or more of these neurotransmitters Each area of the CNS that is affected is responsible for different sx associated with migraine Activation of Cortex and Thalamus (Head pain) Marcus, DA. Headache Simplified 2008.

Neural Substrates of Migraine Migraine involves dysfunction of brain-stem pathways that normally modulate sensory input. The key pathways for the pain are the trigeminovascular input from the meningeal vessels, which passes through the trigeminal ganglion and synapses on second order neurons in the trigeminocervical complex. These neurons, in turn, project through the quintothalamic tract, and after decussating in the brain stem, form synapses with neurons in the thalamus. There is a reflex connection between neurons in the pons in the superior salivatory nucleus, which results in a cranial parasympathetic outflow that is mediated through the pterygopalatine, otic, and carotid ganglia. This trigeminal–autonomic reflex is present in normal persons 34 and is expressed most strongly in patients with trigeminal–autonomic cephalgias, such as cluster headache and paroxysmal hemicrania; it may be active in migraine. Brain imaging studies suggest that important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus, locus ceruleus, and nucleus raphe magnus. Goadsby et al. (2002). New England Journal of Medicine, 346(4), 257-270.

5-HT1B: vasoconstriction 5-HT1D: peripheral neuronal inhibition Goadsby et al. (2002). New England Journal of Medicine, 346(4), 257-270.

Hypothalamic & Insular Activation During Cluster Headache 9 patients with a history of cluster completed PET for regional cerebral blood flow at rest & following nitroglycerin Participants reported that the symptoms of nitro induced headache and the drug free one were equivalent. There was no evidence of activation of the brain stem (unlike with migraines)! Left: gray matter of hypothalamus. This is on the same side (ipsilateral) as the headache pain. Right: bilateral insula. The insula is a relay of sensory information into the limbic system and is known to play an important part in the regulation of autonomic responses. May et al. (1998). Lancet, 352(9124), 275-278.

Migraine -visual aura                                          Bright shimmering 'stars' seen falling across the image (telischopsia). Bright-edged castellated line (fortification spectrum).                                         Scintilating Scotoma: A blind spot surrounded by a bright starburst. It is often mobile. Loss, blanking or darkening of one half of the field of vision (Hemianopia) hemianopia /hemi·an·o·pia/ (-an-o´pe-ah) defective vision or blindness in half of the visual field of one or both eyes; Although many variations occur, scintillating scotoma usually begins as a spot of flickering light near or in the center of the visual fields, which prevents vision within the scotoma. The scotoma area flickers, but is not dark. An arc of light may gradually enlarge, become more obvious, and may take the form of a definite zigzag pattern, sometimes called a fortification spectrum teichopsia /tei·chop·sia/ (ti-kop´se-ah) the sensation of a luminous appearance before the eyes, with a zigzag, wall-like outline

Migraine -visual aura

Tnx…………