Post traumatic headache can occur after mild, moderate, or severe traumatic brain injury (TBI). The most common symptom is headache, which usually resolves within 3 months but can become chronic. Headaches occurring after TBI are often indistinguishable from primary headache disorders like tension-type headache or migraine. Post traumatic headache accounts for about 4% of all secondary headaches. Treatment involves both pharmacological and non-pharmacological approaches based on the type of headache, and may include abortive medications, prophylactic medications, nerve blocks, trigger point injections, and behavioral therapies. Managing any comorbid conditions is also important for optimal treatment of post traumatic headache.
It is a brief presentation on headache disorders. My reference was mainly Medscape. I mentioned treatment in a concise way so you may want to read up more on that.
Headache is one of the most common disorders seen to occur in all age groups but much more so in women. Broadly headaches can be classified as Primary and Secondary Headaches disorders. Primary Headache disorders have no apparent causative factor and are thought to be interplay between genetic predisposition and environmental provocative factors. The most common by far is Migraine. Secondary headaches are those that result from a cause e.g. Brain Tumor.
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
emergence of autoimmune neuropathies and role of nodal and paranodal regions in their pathophysiology.
Peripheral neuropathies are traditionally categorized into demyelinating or axonal.
dysfunction at nodal/paranodal region key for better understanding of patients with immune mediated neuropathies.
antibodies targeting node and paranode of myelinated nerves have been increasingly detected in patients with immune mediated neuropathies.
have clinical phenotype similar common inflammatory neuropathies like Guillain Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy
they respond poorly to conventional first line immunotherapies like IVIG
This presentation briefs out the approach of dementia assessment in line with consideration of recent advances. Now the pattern of assessment has evolved towards examining each individual domain rather than lobar assessment.
This presentation contains information about Dementia in Young onset. Also it describes the etiologies, clinical feature of common YOD & their management.
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
This presentation contains information about the various Entrapment syndromes of Lower limb in descending order of topography. It also contains information about etiology, clinical features and management of each of these entrapment syndromes with special emphasis on electrodiagnostic confirmation.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Introduction
Post concussion syndrome (PCS) it is a symptom complex that includes
headache, dizziness, neuropsychiatric symptoms, and cognitive impairment after
TBI.
M/C symptom to occur is headache.
Can occur after mild, moderate, or severe TBI, usually resolving within the first
3 months, although a minority develop chronic headaches.
3. Introduction
More common after a mild TBI than more severe injuries.
Headaches occurs variably in 25% to 78% of persons following mild TBI.
Estimates of the relative causes of TBI are as follows: motor vehicle accidents
(45%), falls (30%), occupational accidents (10%), recreational accidents (10%),
and assaults (5%) in USA.
Evans RW: The postconcussion syndrome and the sequelae of mild head injury. In Neurology and Trauma, edn. 2. Edited by Evans RW. New York: Oxford University
Press; 2006:95–128.
4. Introduction
Overall, PTH accounts for approximately 4% of all secondary headaches.
No defining clinical features of PTHAs, other than onset after trauma,
distinctly separate them from other headache disorders.
5. Introduction
Athletes and military personnel.
PTH has been well characterized in soldiers who have sustained mTBI, and has
been estimated to occur in 97.8% of concussed soldiers returning during their
final 3 months of deployment.
A/w multiple somatic complaints with depressive symptoms.
Within any sport, females are prone to develop PTH.
Theeler BJ, Flynn FG, Erickson JC. Headaches after concussion in US soldiers returning from Iraq or Afghanistan. Headache 2010; 50:1262–1272.
6. Classification
According to ICHD 2, headache attributed to head & neck trauma include 7
different secondary headache syndromes
1. Acute PTHA
2. Chronic PTHA
3. Acute headache attributed to whiplash injury
4. Chronic headache attributed to whiplash injury
5. Headache attributed to traumatic intracranial hematoma
6. Postcraniotomy headache
7. Headache attributed to other head & neck trauma
7.
8.
9.
10.
11. Pathophysiology
The trigeminal nerve is the major peripheral nerve for transmitting pain stimuli
of the head.
It contains nociceptive afferents from the anterior scalp, anterior cranium,
face, mouth, teeth, temporomandibular joints, sinuses, cranial blood vessels,
and meninges.
Injury to any of these structures can cause headache.
12. Pathophysiology
The greater and lesser occipital nerves, which arise from the C2 and C3 cervical
spinal roots, convey nociceptive stimuli from the posterior head and scalp.
Painful stimuli from structures of the cervical spine are conveyed largely by the
cervical nerve roots.
13. Pathophysiology
The central processes of
trigeminal pain neurons and
cervical pain neurons converge
within the CNS in the upper
cervical spinal cord.
Pathways collectively is known
as the trigeminocervical
complex.
The trigeminocervical complex
helps explain why injury of
neck structures can cause
headache and vice versa.
14. Pathophysiology
Mild head injury are rarely cause identifiable underlying structural injury.
Number of neuronal biochemical and cellular changes induced by head
trauma.
Changes include widespread neuronal depolarization, indiscriminant release of
glutamate and other neurotransmitters, altered glucose and energy utilization,
and decreased magnesium levels.
15.
16.
17. Pathophysiology
DTI studies have discovered regions of associated axonal swelling in patients
with mild TBI.
SPECT/PET imaging can demonstrate structural and functional deficits.
18. Greater white matter pathology predicted greater cognitive deficits,
suggesting DTI as an objective means for determining the relationship of
cognitive deficits to TBI.
19. Clinical features
PTHAs are highly heterogeneous.
Do not possess any unique clinical symptoms.
The current criteria for PTHA require onset of headache within 7 days of head
or neck trauma, but do not require the presence of any particular headache
characteristics.
20. Clinical features
72% of headaches are bilateral in location.
In one study, a frontal location was seen in 50%, followed by holocranial (18%),
hemicranial (13%), and bitemporal (10%).
Over 80% of PTHAs in civilian populations are nonthrobbing.
Lew HL, Lin PH, Fuh JL, et al. Characteristics and treatment of headache after traumatic brain injury: a focused review. Am J Phys Med Rehabil 2006;85(7):619–627.
21. Clinical features
70 – 96 % headaches developing after head trauma often possess the same
characteristics as primary headache disorders.
Major subgroups of headaches after trauma include tension-type headache,
migraine, cranial neuralgias, cervicogenic headaches, and MOH.
M/C are tension-type headache or migraine headache.
22. Clinical features
33% of PTHAs resemble tension-type headaches with a wide range of 6%-85%.
Bilateral and of mild or moderate severity.
Pressing or tightening in nature and not aggravated by routine physical activity.
May be accompanied by either light or sound sensitivity, but not nausea.
23. Clinical features
28% - 60% of PTHAs resemble migraine.
M/C form of PTHA after military-related mild head trauma.
Moderate or severe, unilateral or asymmetric, throbbing or pulsatile in quality,
aggravated by or cause avoidance of routine physical activity, and accompanied
by either nausea and vomiting or both light and sound sensitivity.
24. Clinical features
Last several hours to several days without treatment.
Visual aura might occur.
Not be distinguishable from idiopathic migraine by clinical features or by
responsiveness to treatment.
25. Clinical features
Rarely, head trauma can precipitate the development of trigeminal autonomic
cephalalgias.
Manifest as unilateral headache accompanied by prominent autonomic
manifestations.
26. Clinical features
Occipital neuralgia is probably the most common neuralgiform disorder
following head or neck injury
Typically presents with persistent, moderate, side-locked unilateral head pain
with episodes of brief, severe, lancinating pain radiating from the occipital area
to the side of the head.
Trigeminal neuralgia is rare.
27. Clinical features
Cervicogenic headaches occur when pain is generated or referred from a
source in the cervical spine, such as cervical discs, facet joints, or myofascial
structures. Located in posterior head. Unilateral/bilateral.
Typically have persistent or intermittent neck discomfort and headaches may
be precipitated by certain neck movements.
Neck or occipital tenderness with or without trigger points may be present.
28. Clinical features
Medication overuse headache, previously called analgesic rebound headache.
Analgesic overuse is defined as use of acute analgesics 15 or more days per
month for more than 3 months.
Of patients with PTHAs, 19% - 42% develop this secondary headache disorder.
M/C in patients with migraine.
29. Clinical features
Usually begins a number of hours after consuming the offending analgesic.
Typically the headaches worsen for 2 weeks after analgesic cessation and then
gradually improve over the next 4 to 6 weeks.
Opioids, combination medications, and triptans - potential to cause MOH
NSAIDS - less likely
Dihydroergotamine and antiemetics - unlikely to induce MOH.
30. CLINICAL EVALUATION
Comprehensive history
Focus on preinjury and postinjury headache pattern.
Physical examination
Brief cognitive assessment
Look for FND
Range of neck movement
Fundus examination
31.
32. Indication for Imaging
LOC greater or equal to 5 seconds
Altered mental status
FND
Progressively worsening headache pattern
Intractable headache
Persistent rhinorrhea
Headache induced by position
33. Other causes of headache after trauma
Dangerous Causes of Headache
CVT Cerebral aneurysm
Subdural / epidural hematoma Skull fracture
ICH Cervical vertebra fracture
SAH Cervical disc protrusion
Carotid or vertebral artery dissection
Carotid-cavernous fistula
34. Imaging
MR or CT angiogram - arterial dissection, aneurysm, vasospasm, or carotid-
cavernous fistula are considerations.
MR or CT venogram - in patients with possible cerebral vein thrombosis.
Cervical spine MRI - suspected cervicogenic headaches
35. Role of Lumbar puncture
Positional headache.
Low CSF pressure which can caused by dural tear.
36. Screening of comorbid condition
Concurrent medical & psychological conditions that can exacerbate headaches.
Common comorbidities include
Sleep disorders Posttraumatic stress disorder (PTSD)
Psychosocial stressors Depression
Alcohol or drug abuse Anxiety
Concurrent physical injuries (e.g, explosive blast injuries with amputation, eye
injury, hearing loss, or polytrauma)
Van Reekum R, Cohen T, Wong J. Can traumatic brain injury cause psychiatric Disorders? J Neuropsychiatry Clin Neurosci 2000;12(3):316–327
37. Screening of comorbid condition
Critical to identify and treat comorbidities to most optimally.
Comorbid conditions may limit headache treatment options or provide
therapeutic opportunities.
To select treatment that simultaneously benefit one or more comorbid
condition.
.
38. Treatment
Challenging and rewarding.
Treatment is based on treatments for phenomenologically similar headaches.
Goal
Abort headache attacks Reduce disability
Decrease headache frequency Prevent chronicity
39. Treatment
The goal is to achieve complete relief or nearly complete relief as rapidly as
possible by abortive agents.
Patients who experience
2 or more moderate-severe headache attacks/week.
3 or more days of impaired activities/month over a period of several months.
Despite use of abortive medications are good candidates for headache
prophylactic agents.
40. Treatment
Prophylactic medications require a minimum of 4 weeks to take effect.
Should begin with low dose to minimize S/E & gradually increased over weeks
or even months.
41.
42. Alternative treatment for acute attacks
Opioid medications are generally not highly effective for most headache types
and should not be used as first-line headache abortive agents.
IV or oral corticosteroids (eg, prednisone 60 mg daily for 5 days),
IV Valproaic acid
IV Magnesium
43.
44.
45.
46.
47. Nonpharmacologic Therapies
1) Behavioural therapies
Uncontrolled studies of cognitive behavioural therapy, relaxation therapy, and
biofeedback have shown favourable results in PTHA
2) Life style modification like healthy meal, sleep, exercise patterns, to avoid
triggers for headache, to avoid caffine overuse, smoking, alcohol.
Gurr B, Coetzer BR. The effectiveness of cognitive-behavioral therapy for post-traumatic headaches. Brain Inj 2005;19(7):481–491.
48. Nonpharmacologic Therapies
3) Physical modalities
Physical therapy, osteopathic manipulation therapy, acupuncture.
More useful as an adjuncts to medical therapy particularly in patients with
suspected cervical sources of pain.
49. Injections & Procedures
Nerve blocks
Occipital nerve blocks - occipital neuralgia.
One case series showed an 80% response rate of PTHA following occipital nerve
blockade.
Other Common sites include auriculotemporal nerve, supraorbital nerve,
supratrochlear nerve, sphenopalatine ganglion.
Blocking a single nerve unilaterally or bilaterally or blocking multiple nerves.
Hecht JS. Occipital nerve blocks in postconcussive headaches: a retrospective review and report of ten patients. J Head Trauma Rehabil 2004;19(1):58–71.
50. Arch Phys Med Rehabilitation 2004;85:1013-6.
We present a case wherein a man in his late twenties with posttraumatic headache
obtained more than 17 months of relief with SPG pulsed-mode radiofrequency
lesioning.
SPG pulsed-mode radiofrequency is a nonablative, neural lesioning method that
may be useful in the treatment of posttraumatic headache.
51. Injections & Procedures
Headaches secondary to C2-C3, C3-C4 facet joint dysfunction can be treated
with facet joint blocks or cervical medial branch blocks for cervicogenic
headache.
Trigger point injections are very useful in cervicogenic headache.
Occipital neurolysis, occipital nerve decompression surgery, and implantation
of occipital nerve stimulator are potentially useful treatments but studies are
required.
55. Trial based therapy
Use of melatonin in children with persistent PTH at doses of 3 to 10 mg has
demonstrated positive effects in up to 75% of participants in one study
population.
Kuczynski A, Crawford S, Bodell L, Dewey D, Barlow KM. Characteristics of post-traumatic headaches in children following mild traumatic brain injury and their
response to treatment: a prospective cohort. Dev Med Child Neurol. 2013;55(7):636-641.
56. 30/M, fell down from
motorcycle.
LOC for 30 minutes
Confusion and amnesia for 7
days
Disequilibrium and vertigo,
holocranial throbbing
headache with photo and
phonophobia with associated
nausea,vomiting after he was
discharged.
Started on ibuprofen &
paracetamol.
All symptoms improved in 6
weeks. He joined job in 2
months.
57. A 35-year-old male army officer
Hit his helmeted head on the roof of a military vehicle after it was struck by an
explosive device in Iraq.
Multiple prior concussions from intramural football and a parachute injury.
Left retro-orbital, dull, constant pain, worsening with movement, associated
with photosensitivity, phonosensitivity, nausea, and blurred vision.
Chronic neck and low back pain, poor balance, poor concentration,
forgetfulness, difficulty making decisions, slowed thinking, anxiety, depressed
mood, difficulty falling or staying asleep, repeated disturbing memories,
nightmares, and angry outbursts.
58. Cervical tenderness on examination with C-spine MRI showing degenerative
changes with normal MRI brain.
Treated with zolmitriptan 5mg for acute attacks, prednisolone for 10 days,
nortryptiline 10mg bedtime.
Gabapentin maximum dose was added gradually followed by botulinum toxin (
bilateral frontalis, corrugators, temporalis, splenius capitis, midcervical
paraspinal, lumbar paraspinal areas).
Behaviour therapy was continued for PTSD during this period.
59. References
1. Jay c. Erickson et al., Posttraumatic headache, continuum lifelong learning neurol
2010;16(6):55–78.
2. Bert b. Vargas et al., Posttraumatic headache, curr opin neurol 2012, 25:284–289.
3. Raquel langdon et al., Posttraumatic headache, pediatric annals, vol. 47, no. 2, 2018.
4. Mark obermann et al., An update on the management of posttraumatic headache,
therapeutic advances in neurological disorders, 2015, vol. 8(6) 311– 315
5. Francis x. Conidi et al., Understanding posttraumatic headache, part 2: management
and treatment, practical neurology, september 2017.
1)An inverse relationship exists between the severity of head injury and incidence of PTHA.
1)Headaches tend to occur more frequently and are more likely to persist after mild head injury compared to moderate or severe head injury.
1)Of 377 patients with severe head trauma, only 4% to 23% had headaches 1 year later.
International classification of headache disorders
A number of risk factors for developing chronic PTHA have been identified.
These include female sex, lower educational level, low socioeconomic status, prior history of headaches, mild severity of head trauma, short duration of posttraumatic amnesia, and medication overuse.
In comparison to extracranial injuries (ECI), such as a bone fracture, mTBI patients are more likely to have persistent symptoms after 3 months
The current classification criteria for PTHAs do not include the characteristics or accompanying features of the pain or the specific cause of injury (eg, blunt impact, explosive blast).
Moreover, the time criteria are somewhat arbitrary and not based on pathophysiologic mechanisms.
The central processes of trigeminal pain neurons and cervical pain neurons converge within the CNS in the upper cervical spinal cord.
Pathways collectively is known as the trigeminocervical complex.
2) A number of neuronal biochemical and cellular changes induced by head trauma have been identified and may contribute to the development of PTHAs in the absence of identifiable structural injury.
Early studies demonstrated that biomechanical injury results in ionic flux and hyperacute indiscriminate glutamate release.
Potassium efflux, and sodium and calcium influx, occur due to damage to lipid membrane.
Initial ionic flux and depolarization can then trigger voltage- or ligand-gated ion channels, creating a diffuse ‘spreading depression-like’ state that may be the biological substrate for very acute post-concussive impairments.
2) Do not possess any unique clinical symptoms that clearly distinguish them from nontraumatic headache disorders.
If premorbid headaches existed, the preexisting headache type (ie, migraine) is usually magnified after head injury.
Most children who sustain a mTBI recover within a few weeks.
autonomic manifestations, such as conjunctival injection, lacrimation, ptosis, miosis, eyelid edema, rhinorrhea, or facial sweating abnormalities
MOH develops in susceptible patients when frequent use of acute analgesic medication is continue over a prolonged period of time.
1)The patient becomes trapped in a cycle of escalating headaches and increasing medication use.
BESS An error is defined as opening the eyes, lifting the hands off of the hips, stepping, stumbling or falling out of position, lifting the forefoot/heel, abducting the hip by >30 degrees, or failing to return to test position in under 5 seconds.
Designed for objective measure of assessing static postural stability after mild TBI and to assist in return to sports play decisions.
triggered by moving to an upright posture and relieved by lying back to supine position.
In an analysis of 10 studies, the prevalence of major depression after TBI was 44%.
The incidence of PTSD appears to be inversely related to the severity of the injury. In one study, the incidence of PTSD was 27% among patients who had less than 1 hour of loss
of consciousness compared to only 3% among those who were unconscious for more than 12 hours
All these comorbid conditions are risk factors for prolonged recovery of headache.so need to be addressed.
1)To date, no randomized, controlled clinical trials evaluating the efficacy of any therapies for PTHAs have been done. No US –FDA approved medication.
2)Classify headache.
Most practitioners do not initiate prophylactic therapy in the acute or early subacute stage because many patients with PTHAs experience spontaneous resolution in the first month or two after injury.
many practitioners would agree that patients who continue to experience frequent headache more than 2 months after the injury are appropriate candidates for prophylactic therapy.
3) until the frequency of headaches decreases, side effects develop, or the highest target dose is reached
3) Switching prophylactic agents prematurely, without first titrating up the dose or treating for a minimum of 6 weeks, should be avoided.
.
Lamotrigine is another option for neuralgiform headache, being well tolerated with minimal adverse cognitive side effects, but the dose must be slowly titrated up to minimize the risk of a serious mucocutaneous reaction.
A good musculoskeletal exam looking for trigger points, tenderness over the spinous processes, and decreased range of motion should be part of the initial evaluation.
Trigger points of the head and neck are often associated with various headache disorders.
a combination of physical medicine and trigger point injections may help to lower the patient’s headache frequency.
Cessation of analgesic medication inevitably results in worsening daily headaches for about 2 weeks followed by a gradual improvement back to an episodic headache pattern within 6 weeks.
Sleep-inducing medication and adequate hydration may be helpful during the withdrawal period.
Counselling has to be done on same visit when patient has been advised for medical management which increase the effectiveness of medication.
No RCT have evaluated the effectiveness of any of these approaches for PTHAs, but evidence supports their use in other headache disorders. Can be used as an adjunct to pharmacological treatments.
1) Life style modifi
Have not been fully evaluated for PTHA
3) Typical anesthetics include bupivacaine (0.25% to 0.75%) or lidocaine (2%), with volumes ranging from 0.5 to 2cc per site.
can be given alone, combined with each other and/or with a steroid, usually triamcinolone.
Moderate to severe injury with positive images findings.
Improved completely in 6 weeks.
Prognosis is good for headache after moderate to severe injury.
Learning points
Headache onset after multiple bouts of mild head injury
Persistent of chronic headache despite mild severity of head injury
Presence of PTSD, insomnia, neck and back pain exacerbated headache syndrome
Multidisciplinary approach for chronic headache.