cluster headache

Mechanism and novel approaches to treatment of cluster headache

Virginia Thornley, M.D., Neurologist
January 2, 2019
Cluster headache is a debilitating neurological condition which may be difficult to control. Novel approaches to treatment have been explored because of its refractory response to treatment.
Mechanisms involved in cluster headache
The pathophysiology involves the trigeminovascular pathway. This involves innervation to the  cerebral blood vessels and trigeminal complex including the nerves and ganglion. The ganglion has connections with the blood vessels of the cerebrum, the trigeminocervical complex and the dorsal horns of the C1 and C2 levels. In cluster headaches, certain chemicals are found to be increased during an attack  including calcitonin gene-related peptide and neurokinins which are neuropeptide vasodilators (1).
Calcitonin gene-related peptide antibody therapies
Some of the new anti-CGRP (calcitonin gene-related peptide antibody) therapies recently introduced to migraine patients have been applied to patients with cluster headache, including fremazunab and galcanezumab (2). it has been found that CGRP is released from the trigeminal ganglion and its transcription is increased when there are conditions that mimic those of migraine which includes an neurogenic inflammatory state (3).
There has been some success in its treatment although its application is not yet indicated for these drugs (2).
Botulinum toxin injection
Injection of onabotulinum toxin into the sphenopalatine ganglion was studied in 7 patients with chronic cluster headache. Of these, 3 dropped out. The patients were followed 24 months. There was a 50% reduction in occurrence of pain, after repeated injections. Due to the small size results should be interpreted with caution, however, because of repeated injections, its effectiveness may be significantly underestimated. This is a small pilot observational study. Larger studies are needed (4).
 
Vagal nerve stimulation
Vagal nerve stimulation was employed in 30 patients and a mean reduction of 26 attacks/week to 9.5 over a 3-6 month period was seen. Mean attack duration was 51.9 to 29.5 minutes. Larger studies are needed (5).
In summary 
Several new novel approaches include vagal nerve stimulation and botulinum toxin injections. Anti-CGRP antibodies are another novel treatment but have not yet been submitted for an indication. Larger studies are needed.
@VThornley_MD
Reference
  1. Goadsby, P.J., Edvinson, L., Human in vivo evidence for trigeminovascular activation in cluster headache.Neuropeptude chanes and effects of acute attackes therapies. Brain. 1994 Jun; 117 (Pt 3):427-34
  2. Ashehoug, I., Bratbak, D.F., Tronvik, E.A. Long-term outcome of patients with intractable chronic cluster headache treated with injection of onabotulinumtoxin A toward the sphenopalatine ganglion – an observational study. Headache, 2018, Nov; 58(10):1519-1529
  3. P.L. Durham, Calcitonin gene-related peptide and migraine. 2006, Jun. 46 (Suppl 1):S3-S8
  4. Tepper, S.J. Anti-calcitonin gene-related peptide (CGRP) therapies: update on a previous review after the American Headache Society 60th Scientific Meeting, San Francisco, June 2018
  5. Marin, J., Giffin, N., Consiglio, E., mcClure, C., Liebler, E., Davies, B. Non-invasive vagus nerve stimulation for treatment of cluster headache: early UK clinical experience. J. Headache Pain. 2018, Nov. 23; 19

Disclaimer: This is for informational purposes only and is not medical advice. Please see your physician. Reading this does not constitute a physician-patient relationship.

Standard
Closed head injury

Closed head injury: electroencephalographic changes in post-concussive syndrome

Virginia Thornley, M.D., Neurologist, Epileptologist

March 10, 2018

Introduction

A concussion occurs commonly as high-speed vehicular accidents become more common in today’s fast-paced world. In addition, it occurs frequently in sports-related activity such as football or boxing. The brain is composed of millions of connections and though a patient may complain of several neurological complaints, it is not often manifest in neuroimaging studies, except perhaps diffusion tensor imaging. More often than not, a good clinician can diagnose symptoms of post-concussion syndrome based on neurological symptoms and a preceding event. During injury, there is shearing of thousands of axons diffusely throughout the brain. The contrecoup effect of the injury occurring over the frontotemporal poles produces damage causing a myriad of neurological symptoms. On EEG, non-specific changes can be found corresponding with the degree of injury. There is slowing of the posterior dominant rhythm and excessive theta rhythms which eventually clears after weeks or months of recovery (1).  Some patients, however, are left with recurrent symptoms such as post-concussion headaches, or dizziness or sensations of discomfort. On EEG, some studies show post-concussion symptoms correlating with bursts of theta rhythms.

barcelona 1 239_preview

EEG findings in a few minutes spanning more than 6 months

In animal studies, the EEG shows high voltage sharp waves followed by diffuse background suppression which can last a few minutes. This is followed by diffuse slowing that normalizes after 15 minutes in one study occurring between 10-60 minutes (2). Over a few hours to weeks, there are increased theta and delta rhythms and reduced ratio of theta to alpha frequencies. there was an increase in delta activity in the posterior regions. There are brief periods of reduced delta: alpha ratios. In one study called the “Belfast studies,” amnesia was evaluated in 73 patients at 24 hours and 6-week follow-up with EEG and brainstem auditory evoked potentials (BAEP). It was found that amnesia did not have EEG correlate but correlated with abnormal BAEPs suggesting amnesia was derived from brainstem dysfunction rather than cortical dysfunction. Over weeks to months, there are reduced alpha and increased delta rhythms are noted. In the Belfast studies, there was more persistent left temporal slowing, which seemed to correlate with chronic symptoms when it persisted beyond 6 months. After more than 6 months, there were increased delta activity and fewer alpha rhythms (2).

Other EEG findings in closed head injury and part-seizure like activity

In one retrospective study of 3 groups of veterans at a Veteran Affairs Medical Center,  30 comprised of normal subjects with normal EEGs, 30 had EEG’s with non-paroxysmal theta delta slowing and 38 patients had theta bursts. The patients with episodes of theta bursts seemed to have corresponding partial seizure-like clinical symptoms. Patients with head injury reported episodic symptoms across all 3 groups. These findings conclude that clinicians may want to evaluate patients for seizure-like activity in the context of closed head injury and presence of bursts of theta activity (3).

barcelona 1 159_preview

Introduction/Disclaimer

https://neurologybuzz.com/

About

Reference

  1. Nuwer, et al, “Routine and quantitative EEG in mild traumatic brain injury,” Clinical Neurophysiology, 2005, Sep., 116(9):2001-2025
  2. Haneef, et al, “Electroencephalography and quantitative electroencephalography in mild traumatic brain injury,” Journal of Neurotrauma, 2013, Apr., 30(8):653-656.
  3. Roberts, et al, “Theta bursts, closed head injury, and partial seizure-like symptoms: a retrospective study,” Applied Neuropsychology, 2001, 8(3):140-7.
Standard
migraine

Migraine:Non-Pharmacologic Ways to Deal with Migraines

By Virginia Thornley, M.D., Neurologist
February 15, 2018

Introduction
Migraines are characterized by recurrent pounding, throbbing pain, occurring on one side of the head. At times, it alternates.  At its highest intensity, it is rated a 10/10 on the pain scale. It is often accompanied by nausea, vomiting, sensitivity to bright lights and loud noises. It may or may not be accompanied by visual symptoms which can range from seeing bright lights to seeing sophisticated patterns of color called fortifications that often migrate across your visual fields. The frequency may vary from infrequent to a daily basis. Some patients may have other neurological symptoms that accompany it, however, migraine is a diagnosis of exclusion. In other words, other more serious causes are ruled out before a diagnosis of migraine can be concluded if you also experience other neurological symptoms. It is important to be fully evaluated by a neurologist to exclude other possible neurological etiologies.

Lifestyle changes that help reduce migraine frequency
There are non-pharmacologic measures which may reduce the frequency of migraines. Oftentimes, triggers can be found. Lifestyle changes are the hardest to do but they greatly minimize the frequency of migraines.

Avoidance of caffeine
If large amounts of coffee are consumed, tapering can help ease into complete cessation. A sudden cessation may result in withdrawal effects of caffeine which can involve headaches. Common sources of caffeine include coffee, tea, soda, and chocolate. Avoidance of beverages labeled as decaffeinated as there is still a small amount of caffeine is also beneficial.

There is a lot of myth and misinformation. Many migraineurs say that caffeine alleviates their headaches. Caffeine can help a migraine in the short-term, however, it prolongs a migraine cycle. Refer to a neurologist for questions.

10599125_10152611750993841_341083211321527463_n

Obtain adequate sleep
Adequate rest at night is important. This may vary from 6-8 hours. A rule of thumb is if one cannot drag themselves out of bed sleep is inadequate.  Adequate sleep means waking up refreshed. Sleep requirements vary per individual. Sleep deprivation propagates the migraine cycle. Sleep must be continuous and nocturnal allowing the body to enter the restorative deep wave sleep at stages 3 and 4 of sleep. Even if prolonged sleep occurs if constantly interrupted one will not wake up refreshed since the natural sleep cycle is disrupted and only light sleep stages 1 and 2 will occur. It should be nocturnal, the body is designed to sleep at night when hormones are secreted, daytime sleep will not have the same quality.

Avoidance of food triggers
A food journal provides much useful information. Common culprits include wine, cheese, hot dogs, and fish. Certain red meat may trigger migraine. Food triggers vary per patient and are unique to each individual.

10599125_10152611750993841_341083211321527463_n

Avoidance of excessive use of over the counter medications
Over the counter medications are easily accessible and consumable. A common pitfall is to overuse these medications. When stopped abruptly, rebound headache may result. It is not infrequent for patients with migraine headaches to have rebound headaches compounding the condition.

Magnesium use
Magnesium is known to help with migraine. Intravenous magnesium is often used in the hospital setting in status migrainosus which is a continuous extremely painful migraine which sometimes lasts up to weeks. Magnesium is a mineral found naturally in food. Oral magnesium oxide at specific doses is helpful in preventing the migraine cycle.

Riboflavin use
Riboflavin is found naturally in the diet. It can prevent the migraine cycle at specific doses.

Other lifestyle changes
Other lifestyle changes include keeping hydrated especially during hot weather, eating 3 meals a day and avoiding hunger. Some triggers are unique to individuals. Avoiding stress helps with migraines. A zen-like environment is optimal.

Medications are often prescribed for the management of frequent migraine headaches. They are divided into 2 classes, preventative and abortive agents. However, even the best medications will not work effectively if triggers or aggravating factors are still present as mentioned above in daily life.

Introduction/Disclaimer

About

https://neurologybuzz.com/

Standard