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

2. 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?

3. 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

4. What causes Hedache?

5. What are common causes?

6. 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
Migraine
Headache ? Cause
Post-traumatic
Facial pain ?cause
Depression
Trigeminal neuralgia
Cluster headache
Malignant IC Tumour
Benign IC Tumour 9
Temporal arteritis 6
Post-herpetic neuralgia 5
Benign IC hypertension 4
Cough headache 3
Subdural haematoma 2
Sinus infection 1

7. Headache Diagnosis and Testing

12. 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

13. 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.

15. Autonomi c Cephalgias

16. 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

17. 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.

18. 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),

19. 5-HT1B: vasoconstriction 5-HT1D: peripheral neuronal inhibition
Goadsby et al. (2002). New England Journal of Medicine, 346(4),

20. 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),

28. 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

29. Migraine -visual aura

50. Tnx…………