Download Free Medical Headaches in Children and Adolescents PowerPoint Presentation

Headaches in Children and Adolescents PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Headaches in Children and Adolescents" by Johanan Levine, MD.
This medical PowerPoint presentation talks about headaches as a common problem among children and adolescents.
There are many types of headaches, including tension headaches, migraines, and cluster headaches, among others. The causes of headaches in children and adolescents can vary and may include stress, lack of sleep, dehydration, eye strain, sinus infections, and more serious conditions such as brain tumors.

Tags : Headache in pediatrics, pediatric patients, tension headaches, migraines, sinus infections, Child Neurology PowerPoint presentation, Neurology PowerPoint presentation

Published on : Mar 21, 2023 | Views : 810 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Headaches in Children and Adolescents Johanan Levine, M.D
Slide 2-

INTRODUCTION (1) Headaches (HA) are common in children HA may be secondary if directly related to an underlying cause or primary if no other cause than the headache disorder is found Migraine is the most prevalent cause of recurrent disabling headaches Standardized criteria are used in diagnosis Abnormal exam correlates with pathology
Slide 3-

INTRODUCTION (2) It is most important to promote agreement, understanding and cooperation of the patient and family with any treatment plan Treatment strategies (and goals) include: Acute therapy (prompt complete relief or rescue, avoiding medication overuse) Preventative therapy (reduce pain frequency and improve function, quality of life (QOL)) Behavioral approaches (healthy habits)
Slide 4-

EPIDEMIOLOGY (1) 20% of primary care visits are for HA 90% of headache referral center patients have migraine and over 90% of those referred to a neurologist have migraine Bille (1962): 39% have HA by age 6, 70% by age 15 in Sweden; other studies, up to 82% of children Family history plays a strong role (genes for familial hemiplegic migraine mapped)
Slide 5-

EPIDEMIOLOGY (2) In childhood sex ratios of migraine are equal but after 15 years of age female:male::2;1 More prevalent in North America than Europe and least in Africa 10% have <1 migraine per month, 32% have1, 40% have 2-4 per month and 18% of those with migraine have >4 per month
Slide 6-

EPIDEMIOLOGY (3) Migraine most prevalent in the poorest but does not decrease much from lower middle class to upper class income people Half of migraineurs account for 90% of the time lost from work due to migraine Stroke, epilepsy, depression, mania, anxiety, panic disorders coexist with migraine more commonly than by chance
Slide 7-

EPIDEMIOLOGY (4) In teenagers with migraine, there are many who suffer prolonged attacks (of 72 hours or more) Migraine is one of the most common disorders of childhood
Slide 8-

CLASSIFICATION (1) Secondary HA disorders are those caused by another etiology: Traumatic HA (acute, chronic, whiplash) Vascular HA (stroke, AVM, CCM, cerebral hemorrhage, vasculitis/arteritis) Nonvascular intracranial processes (idiopathic intracranial hypertension with papilledema, other causes of intracranial hypertension, low CSF pressure, noninfectious inflammatory disease, and intracranial neoplasm)
Slide 9-

CLASSIFICATION (2) Substance abuse or withdrawal headaches (such as hangover, medication overuse HA) Infection-related HA often with fever HA due to disorders of homeostasis (dialysis, hypercapnea, arterial hypertension, pheochromocytoma, eclampsia, fasting hypothyroidism HA due to skull, ear, nose, throat, eyes, sinuses, teeth, mouth or facial structures HA due to psychiatric disorders
Slide 10-

CLASSIFICATION (3) Primary headache disorders include: Migraine without aura Migraine with aura (including typical aura with headache, typical aura without headache, basilar-type migraine and familial hemiplegic migraine) and retinal migraine Childhood periodic syndromes (cyclic vomiting, abdominal migraine, benign paroxysmal vertigo of childhood
Slide 11-

CLASSIFICATION (4) Complications of migraine (chronic migraine, status migrainosus, migrainous infarction, migraine-triggered seizure) Tension-type headache Cluster headache and trigeminal autonomic cephalgias Stabbing HA, cough HA, exert ional HA, preorgasmic HA, orgasmic HA, hypnic HA
Slide 12-

CLASSIFICATION (5) The 2004 International Headache Society classification, for instance, defines criteria for pediatric migraine without aura: A. Five or more attacks B. Each lasting one to 72 hours C. Each with at least 2 of 4 features Either bilateral or unilateral (frontal/temporal) Pulsating quality Moderate to severe intensity Aggravated by routine physical activities
Slide 13-

CLASSIFICATION (6) D. At least one of the following two features: Nausea and/or vomiting Photophobia and phonophobia (may be inferred from their behavior)
Slide 14-

PATHOPHYSIOLOGY (1) In migraine, intracranial vessels dilate This activates perivascular sensory trigeminal nerves via serotonin (5-HT)1D receptors to release vasoactive neuropeptides (VANP) VANP worsen vasodilation and create a vicious cycle of vasodilation and pain Pain impulses are transmitted to brainstem via 5-HT1D receptors in trigeminal nucleus in upper cervical cord and brainstem Pain impulses ascend to thalamus and higher cortical centers
Slide 15-

PATHOPHYSIOLOGY (2) Hence, as ortho- and antidromic trigeminal vascular and pain fibers contribute to the pain, their modification by 5-HT1B active triptans may counteract both the pain and the vasodilation Genetic factors seem to contribute to sensitivity to specific neurotransmitters; familial hemiplegic migraine mutations alter channels
Slide 16-

DIFFERENTIAL DIAGNOSIS (1) Migraines are often unilateral, throbbing, supraorbital, temporal and with (or without auras or complicating deficits) Tension-type may be circumferential, tight Tumors may give focal deficits. Tumors, abscesses, hydrocephalus and idiopathic intracranial hypertension may produce signs such as papilledema or VIth nerve palsy
Slide 17-

DIFFERENTIAL DIAGNOSIS (2) Infections often produce meningismus as does subarachnoid bleeding Vascular lesions or ruptures often produce a dramatically acute severe headache with deficits
Slide 18-

EVALUATION (1) Detailed prior medical history including illness, traumas, exposures, toxins, treatment trials, doses, effects, side effects, prior studies and family history, and psychiatric/emotional stressors A detailed history of the headaches themselves including quality, location, frequency, duration, triggers (exposures, foods, menses, activities, sex), associated deficits (visual, motor, sensory), nausea, vomiting, photophobia, phonophobia
Slide 19-

EVALUATION (2) The thoroughness of the history and the detail often build confidence, especially as dangerous those who have failed prior treatment often feel shortchanged An examination of vital signs including blood pressure, head and cranial structures, eyes, ears, sinuses, teeth, chest, heart, neck, lymph nodes, pulses, abdomen, back, extremities, and skin is essential to the differential diagnosis
Slide 20-

EVALUATION (3) Missing the cause of secondary headaches is dangerous. Thorough neurological examination is requisite to seek psychological/psychiatric disease, focal deficits, diffuse nerve or muscle disorders, respiratory irregularity or insufficiency, and, especially, meningeal signs and signs of intracranial hypertension
Slide 21-

IMAGING (1) MRI of brain or CT is generally done in acute setting with new onset headaches With recurrent headaches of over a few month’s course, imaging studies are of low yield except where other features of history or examination (if done punctiliously) point in the direction of pathology.
Slide 22-

IMAGING (2) Magnetic Resonance Imaging of everyone with a headache disorder is wasteful but reassuring and protective against lawsuits; the reassurance certainly can help in treating headaches and in gaining patient confidence. Imaging hardly anyone is cost effective but less reassuring; it does avoid false positive MRI white matter findings
Slide 23-

IMAGING (3) The 2002 guidelines on LP, EEG and MRI of the American Academy of Neurology (AAN) and the Child Neurology Society (CNS) emphasize the need for MRI when history or examination point in that direction and find no indication for the others absent other symptoms or signs than the headache alone
Slide 24-

IMAGING (4) MRI in those with headaches with trauma, rigid neck, examination focally abnormal, altered mental status, new onset or worst headache 50% of children with brain tumors have headaches; only17% have the classic early morning headache and vomiting Headache features which should lead to imaging in children: worst of life, HA on exertion, early AM onset, progressive worsening, fever, meningismus, focal deficits, worse with Valsalva
Slide 25-

IMAGING (5) MRI has no ionizing radiation and is more sensitive to subtle lesions especially in the posterior fossa; it takes longer, may require sedation and cannot be doe with pacemakers, cochlear implants. CT is good for acute blood, quicker but less sensitive for tumors or abscesses or chronic changes or subtle malformations and migrational disorders
Slide 26-

TREATMENT-PHILOSOPHY Involve the patient in making the long-term plan Create realistic goals especially as regards medication overuse Be flexible and sensitive to the patient’s wishes Be prepared to discuss unproven therapies Combine behavioral, physical, and drug
Slide 27-

TREATMENT-NONPHARMACOLOGICAL Treating comorbid conditions of mood, anxiety with therapy may help headaches Relaxation training and biofeedback can be useful in migraine and tension-type HA in children even in early school age years This may avoid medication overuse headaches Ascertaining and avoiding triggers, toxins
Slide 28-

TREATMENT-ALTERNATIVE MEDICINE Small studies mostly in adults have shown some benefit from Riboflavin, Magnesium (up to 400mg/day), feverfew (unknown doses), melatonin and parasites hybridis Unproven (needing further research): acupuncture, cervical manipulation (potentially dangerous), hyperbaric oxygen, hypnosis, occlusal adjustments, TENS
Slide 29-

TREATMENT-ACUTE ATTACKS/RESCUE (1) AAN 2004 practice parameter for migraine in children and adolescents: Treat rapidly and consistently Restore ability to function Minimize the use of back-up and rescue drugs Only ibuprofen among analgesics and possibly acetaminophen and sumatriptan nasal spray have proven efficacy
Slide 30-

TREATMENT-ACUTE ATTACKS/RESCUE (2) Other options used include metclorpropamide, narcotics (Stadol nasal spray) , and IV valproic acid to stop a HA but each with a risk (movement disorder, habituation or liver toxicity) Other triptans may be effective in some children but not proved; ergot, isometheptane mucate and caffeine-containing combinations may be overused
Slide 31-

TREATMENT-MEDICATION OVERUSE HA As long as analgesics or even triptans are used over 4 days per week, headaches persist and can become daily or every-other-day If a patient can limit intake the chronic daily HA may subside and preventative therapy may help Sometimes hospitalization and IV ergotamine may be needed
Slide 32-

TREATMENT-PREVENTIVE (1) Many drugs have been tried for migraine prophylaxis in children including clonidine, propranolol, topiramate, valproic acid, amitriptyline, trazadone, cyproheptadine, nimodipine, pizotifen, timolol. In some studies, propranolol was effective, in others not so. Flunarizine, a calcium channel blocker not available in the US is seemingly helpful
Slide 33-

TREATMENT-PREVENTIVE (2) However, Flunarizine may induce parkinsonism. Despite years of use there insufficient evidence to make any recommendation about cyproheptadine, amitriptyline, valproic acid, topiramate and levetiracetam for preventive therapy in children
Slide 34-

IDIOPATHIC INTRACRANIAL HYPERTENSION (1) “Pseudotumor cerebri” is often without known cause. Often headache and papilledema are a monophasic illness most prevalent in young obese women or girls. Vitamins, antibiotics, hormones, calcum imbalance, lupus, infections may induce it Venous sinus thrombosis may mimic it even without papilledema
Slide 35-

IDIOPATHIC INTRACRANIAL HYPERTENSION (2) Increased intravascular volume may be reponsible even when no venous sinus thrombosis is detected As many as 15% will lose vision from optic nerve damage if untreated Here, MRI (to look for mass and/or compressed ventricles), MR venography and lumbar puncture (possibly therapeutic) are needed
Slide 36-

IDIOPATHIC INTRACRANIAL HYPERTENSION (3) Diuretics such as acetazolamide (carbonic anhydrase inhibitor) decrease CSF production and lower ICP Lumbar-peritoneal shunt sometimes works Defenestrating the swollen optic nerves surgically also may protect vision
Slide 37-

LOW CSF PRESSURE HEADACHES CSF leak or failure of CSF production, like a leak from a lumbar puncture site can produce a pounding postural headache This improves with lying down but resumes on sitting up MRI may show severely Gadolinium-enhancing meninges Hydration, positioning, blood patch as well as dural patch may decrease HA