Neurological and/or neurovascular components of the major types of headaches
Introduction
Headaches are classified as one of the most renowned neurological complaints. At some point in life, most people experience headaches, and the World Health Organization (WHO) consider the phenomenon as the most disabling condition because of the harmful effects on the quality of life. According to Winn (2011), headache is a common physical manifestation of Traumatic Brain Injury (TBI) and either produce either new primary symptoms or worsen pre-existing symptoms in patients with a prior headache history. The International Classification of Headache Disorders (ICHD) provides a clinical criterion that categorizes headaches into either primary or secondary headaches. More specifically, primary headaches are not linked to any diseases or structural disturbance and are usually benign. Secondary headaches, on the other hand, are less frequent and can be fatal as they are associated with pre-existing conditions such as an infection, tumour, injury etc. The essay discusses the neurological components of the major types of headaches and how pain related to headaches may be misinterpreted as dental pain.
The categories of primary headaches encompass tension-type headache (TTH), migraine, and trigeminal autonomic cephalalgias (TACs). Paroxysmal hemicranias and cluster headaches are forms of primary neurovascular headache which manifest excruciating pain and share some form of circadian, circannual or cycling alongside prominent activation of the cranial parasympathetic autonomic innervation (Brandt et al., 2003). These headaches are to some extent fascinating, but for physicians, they signify a substantial chance for successful therapeutic intervention. Brandt et al. (2003) claim that primary headaches associated with prominent cranial parasympathetic features should be perceived together pathophysiologically as the trigeminal-autonomic cephalalgias (TAC).
The clinical aspect of cluster headache, as outlined by ICHD, is characterized by sporadic, recurrent, short-lived attacks of severe unilateral pain that is often recounted to occur behind or over the eye. These aspects are normally linked to autonomic features like nasal congestion, lacrimation, conjunctival injection and Horner's syndrome; the repeated attacks can occur up to eight times a day and last from 15min to 3 hours. The patients are either classified as episodic cluster headache, which takes up to six weeks and chronic cluster headache for those without substantial breaks. Cluster headache is challenging to treat since it is often resistant to simpler treatments (Edvinsson & Uddman, 2005).
On the principles of therapy, cluster headache has a high probability of being wrongly diagnosed as vascular headache since it can be attributed to the process of inflation in the tributary veins, cavernous sinus, or the pericarotid pathological process. Notably, MRI imaging has failed to reveal the pathological change in the cavernous sinus during active bouts making it challenging to differentiate cluster headache from paroxysmal hemicranias or migraine. However, the Position Emission Tomography (PET) provides a logical basis to understand acute cluster headache in terms of brain dysfunction. The PET can identify two types of pain; the areas only activated by cluster headache and areas involved in pain processing or responses to pain (Brandt et al., 2003).
The biological basis helps physicians to provide effective medical treatments. Acute cluster headache, for instance, can be treated through injection of sumatriptan. Other treatments include methysergide and ergotamine. Long-term prevention of episodic cluster headache includes lithium and verapamil. Important to note, the topiramate drug has proven to be more effective than the rest but also a variety of drugs such as sodium valproate, melatonin, pizotifen, and gabapentin has unproven efficacy (Schwartz & Robbins, 2012). If the pharmacological treatments proposed to fail to treat the patient, the medics could use surgery as the last treatment method but before, they must exploit all the available approaches.
The clinical aspects of paroxysmal hemicranias include female preponderance, short-lasting attacks that take between 2 to 45 minutes, severe unilateral pain, frequent attacks more than five times in 24 hours, and marked autonomic characteristics ipsilateral to the pain. The disorder occurs more in female than men. Regarding the principles of therapy, it is evident that the phenotype of the acute attack is characterized by the trigeminal-autonomic reflex activation (Schwartz & Robbins, 2012). Indomethacin remains the only effective treatment of paroxysmal hemicranias. The indomethacin treatment is administered three times a day at a dosage of 25mg, but if it fails to work, it can be increased to 50mg three times a day dosage. While on indomethacin, most patients will need treatment with H* pump and H2 blockers (Brandt et al., 2013).
On the contrary, secondary headache disorders are less-common and life-threatening headaches caused by an underlying condition that affects the human brain. The causes of secondary headache disorders include brain tumor, disorders of the blood vessels in the brain including stroke, ischemic stroke, hemorrhagic stroke, head injury, increased intracranial pressure, seizures, trigeminal neuralgia, and inflammation from encephalitis, meningitis, and others infections amongst others. The types of secondary headaches disorders include post-traumatic headache, rebound headache, and thunderclap headache. Physicians experience a difficult time when attempting to differentiate between primary and secondary headaches. Apart from checking the vital signs to provide diagnosis, physicians can also blood tests and imaging tests such as MRI, CT scan, and Sinus X-rays.
According to Smith (2018), secondary headaches are relatively less common but life-threatening, accompanied by substantial neuroimaging abnormalities in approximately 1% of the patients that presents with a headache in a clinic. The predictors of intracranial pathology involve having an acute-onset headache, having abnormal neurologic examination findings, and being over 50 years old. SNOOP is an example of screening mnemonics that incorporate these characteristics to help detect secondary etiologies that can lead to mortality and morbidity (Smith, 2018). The successful management of patients with headaches relies on the identification of less severe threatening disorders such as headache associated with hypothyroidism.
The description of secondary headaches usually resembles tension-type headache like glioma, migraines like traumatic brain injury, or a TAC like pituitary adenoma. Thus, recognition of secondary headache would require a thoughtful evaluation of the specific risk-factors like age and comorbidities linked to pulsatile tinnitus symptoms or a thunderclap headache during micturition (Smith, 2018). To identify secondary headaches using the patient history would require a careful examination by the clinician as well as utilization of a diagnostic workup. An independent headache diagnosis would be needed for patients that exhibit a history of episodic migraine caused by either hypothyroidism, sleep apnea, or the overuse of analgesic (Jacobs & Dussor, 2015).
Secondary headache syndromes include giant cell arteritis (GCA), headache attributed to hypothyroidism, and medication-overuse headache. GCA manifests in patients over 50 years with a changed pattern of headache and can be tested using C-reactive protein and erythrocyte sedimentation rate (Rana et al., 2014). Rheumatologists, neurologists, and a headache specialist can help to manage patients with GCA on a long term basis. On the other hand, headache attributed to hypothyroidism would require special education to determine the most effective treatment even though primary care physicians often manage it.
How the pain related to headaches may be misinterpreted as dental pain.
The orofacial pain emanating from neurovascular origin may imitate odontogenic pain to the level that most individuals with trigeminal autonomic cephalgias and migraine can seek dental remedies. According to Nixdorf, Velly & Alonso (2018), more than half of the patients that present with orofacial pain undergo a misdiagnosis with primary dental disorders as they receive misdirected dental medications. Migraine and dental pains have exerted a similar preponderance of complaints. More specifically, migraines without aura that affect the 2nd division of the terminal nerve imitate odontalgia to the point that patients may experience endodontic extraction or therapy. (Nixdorf, Velly & Alonso, 2008) adds that the common features of migraine with or without aura in pericranial tenderness and allodynia may be misconstrued as masticatory musculature pain secondary to a temporomandibular disorder. Therefore, the orthopaedic approaches may lack physiological basis.
Moreover, the intense and localized pain associated with the numerous TACs, especially maxillary or periorbital pain, often causes dental interventions as well as ultimate teeth loss (Alonso & Nixdorf, 2006). Unilateral chronic pain is a risk factor to odontalgia or TMD. Trigeminal Neuralgia and TACs have in the past misdiagnosed as odontalgia due to the location and intensity and the probability to increase the discomfort associated with heightened intracranial pressure (Lopez-Lopez et al., 2012). Furthermore, migraine headaches have also been termed a risk factor of TMD development. Therefore, clinicians need to understand that numerous neurovascular pain disorders, especially migraines and secondary headaches, may exert pain to other tissues. As a result, they should contemplate applying differential diagnosis when the patient present with a pain complaint that appears to be non-odontogenic in nature (Nixdorf, Velly & Alonso, 2008).
Dental clinical scenario
Scenario 1
Summary and complaint
A 60 years old female patient attending regular dental care claims that she has been experiencing severe headache thus requests the dentist to postpone her treatment. She claims that the headaches are severe and present with nausea, dizziness, and blurred vision.
History of complaint
The persistent headaches commenced only two weeks ago. The patient has been unable to establish the causes. She has been managing the pain at times by lying across the bed until the pain disappears. Painkillers from over the counter have not been effective.
Medical history
The 60 years old patient BMI is high because she is overweight. She smoked 10 cigarettes a day for 15 years and drinks 22 units of liquor weekly.
Dental history
The patient has not presented any dental problems in the regular sessions to the dentist. However, she has never complained of tenderness in the muscles of mastication, but attrition from bruxism has been noted.
Assessment
There is a likelihood that migraine can cause headaches with visual disturbance and nausea occasionally. Nonetheless, migraines are common in young and middle age populations and suggesting a diagnosis on a postmenopausal patient would be unusual. The said bruxism is inapt and asymptomatic.
Role of the dentist in the diagnosis and treatment of the headache
The dentist is expected to showcase an extensive understanding of the signs, symptoms, and causes of craniofacial pain. The dentist should focus on excluding pain of local or dental origin. The dentist should not misinterpret pain of dental origin as head and neck pain caused by GCA, trigeminal and other neuralgias as well as chronic idiopathic facial pain.
Scenario 2
An assessment of pain on a group of 50 dental patients was conducted to assess whether pain related to headaches can be misinterpreted as dental pain. The study revealed that patients with acute or chronic dental conditions experienced a moderate-severe level of pain while severe pain was experienced by those with multiple diagnoses (Dai, Ehizele & Enabulele, 2015). However, studies have shown that when an aching tooth is left untreated, individuals can develop migraines. Therefore, pain related to headaches may be misinterpreted as dental pain since it is uncommon for individuals with migraines or tension type headaches to consult a physician when they are experiencing dental pain. This leads to misdiagnosis.
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References
Jacobs, B., & Dussor, G. (2016). Neurovascular contributions to migraine: Moving beyond vasodilation. Neuroscience, 338, 130-144. https://doi.org/10.1016/j.neuroscience.2016.06.012
Lopez-Lopez, J., Garcia-Vicente, L., Jane-Salas, E., Estrugo-Devesa, A., Chimenos-Kustner, E., & Roca-Elias, J. (2012). Orofacial pain of cardiac origin: Review literature and clinical cases. Medicina Oral Patología Oral y Cirugia Bucal, e538-e544. https://doi.org/10.4317/medoral.17636
Nixdorf, D. R., Velly, A. M., & Alonso, A. A. (2008). Neurovascular pains: Implications of migraine for the oral and maxillofacial surgeon. Oral and Maxillofacial Surgery Clinics of North America, 20(2), 221-235. https://doi.org/10.1016/j.coms.2007.12.008
Odai, E. D., Ehizele, A. O., & Enabulele, J. E. (2015). Assessment of pain among a group of Nigerian dental patients. BMC research notes, 8(1), 251.
Rana, A. Q., Saeed, U., Khan, O. A., Qureshi, A. R., & Paul, D. (2014). Giant cell arteritis or tension-type headache?: A differential diagnostic dilemma. Journal of Neurosciences in Rural Practice, 05(04), 409-411. https://doi.org/10.4103/0976-3147.140005
Schwartz, D. P., & Robbins, M. S. (2012). Primary headache disorders and neuro-ophthalmologic manifestations. Eye and Brain, 4, 49.
Smith, J. H. (2018, February). Ruling out secondary headache. Practical Neurology. https://practicalneurology.com/articles/2018-mar-apr/ruling-out-secondary-headache
Winn, H. R. (2011). Youmans neurological surgery E-book. Elsevier Health Sciences.
