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Showing posts with label headache. Show all posts
Showing posts with label headache. Show all posts

Vascular theories of Migraine

It is the most common Migraine is the most common disabling primary headache globally.

12 percent of migraine are Episodic and 1 - 2 percentage is Chronic.Migraine Attacks are typically present with unilateral throbbing headache and it is associated with following  symptoms 

  1. Nausea
  2. Multisensory Hypersensitivity
  3. Marked fatigue.

The diverse symptomatology highlights the complexity of migraine as a whole nervous system disorder involving somatosensory, autonomic, endocrine, and arousal networks

Vascular Theory of Aura in Migrane

In Migraine  there is Hereditary Susceptibility of Brain. There is Abnormal Intracranial and extra-cranial  vascular reactivity to triggers. Aura is followed by Vasoconstriction, ischemia and focal neurological symptoms. Headache is due to Vasodilation and leads to pulsatile headache

What are the Pitfalls in Vascular theory

MRI perfusion study has showed that there is focal hyperemia precedes oligemia during Migraine aura. Perfusion abnormalities need not always match with symptoms of migraine. Oligemia may spread at 3mm/min beyond vascular territory. Headache can occur as that of migraine aura. Vascular theory cannot explain the premonitory phase. There wont be any Diffusion restriction in  MRI doesn’t show  


SUNCT ( short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) is a rare primary headache syndrome that is characterized by severe, unilateral orbital or temporal pain that is stabbing or throbbing in quality. 
Diagnosis of SUNCT and SUNA
  • SUNCT requires at least 20 attacks, lasting for 5–240 s
  • There should be  ipsilateral conjunctival injection and lacrimation
  • The pain of SUNCT/SUNA is unilateral and it may be located anywhere in the head. 
  • Three basic patterns of SUNCT  can be seen 
                Single stabs, which are usually short-lived
                Groups of stabs
                A longer attack with many stabs between which the pain does not completely resolve, thus                   it  gives a “saw-tooth” phenomenon with attacks lasting many minutes.
  • Characteristics feature that lead to a suspected diagnosis of SUNCT are the cutaneous (or other) triggerability of attacks, and there is lack of refractory period to triggering between attacks. 
  • There is lack of a response to indomethacin.
  • Apart from trigeminal sensory disturbance, the neurologic examination is normal in primary SUNCT.
Secondary (Symptomatic) SUNCT
Secondary SUNCT is seen with posterior fossa or pituitary lesions. All patients diagnosed with SUNCT/SUNA should be evaluated with pituitary function tests and a brain MRI 
Differential diagnosis
The diagnosis of SUNCT is sometimes confused with trigeminal neuralgia particularly in first-division TN
But in trigeminal neuralgia there are no cranial autonomic symptoms and there is clear refractory period to triggering 
Treatment  of SUNCT/SUNA
Abortive therapy
Treatment of acute attacks is not a useful concept in SUNCT/SUNA  because the attacks are of such short duration. Intravenous lidocaine, can arrests the symptoms, can be used in hospitalized patients with SUNCT.
Preventive therapy 
Long-term prevention is to minimize disability and hospitalization is the goal of treatment. 
Drugs for prevention
The drug that is most effective for prevention is lamotrigine, 200– 400 mg/d. 
Gabapentin may also be effective.
Carbamazepine, 400–500 mg/day, can  offer modest benefit.
Surgical treatment of SUNCT/SUNA
Surgical approaches used for SUNCT/SUNA is microvascular decompression or destructive trigeminal procedures,they  are seldom useful and often they produce long-term complications. 
Greater occipital nerve injection offers limited benefit in some patients. 

What is Paroxysmal hemicranial headache?

Paroxysmal hemicrania (PH) is characterized by frequent unilateral, severe, short-lasting episodes of headache. Like cluster headache,the pain in PH tends to be retroorbital but may sometimes experienced all over the head and it is associated with autonomic phenomena such as lacrimation and nasal congestion. 
The essential features of PH are given below
  • Unilateral, very severe pain; short-lasting attacks (2–45 min) 
  • Very frequent attacks (usually more than five a day) 
  • Marked autonomic features ipsilateral to the pain
  • Rapid course (<72 h)
  • There is excellent response to indomethacin.
Paroxysmal hemicranias may be 
1.Episodic PH-Patients with remissions are said to have episodic PH, 
2. Chronic PH whereas those with the nonremitting form are said to have chronic PH.
In contrast to cluster headache, which predominantly affects males, the male:female ratio in paroxysmal hemicranias  is close to 1:1.
Treatment of PH
Indomethacin (25–75 mg tid) is the treatment of choice.it can completely suppress attacks of PH
Topiramate is helpful in some cases of PH. 
Piroxicam has been used, but it is not as effective as indomethacin. 
Verapamil, a useful drug for treatment for cluster headache, does not appear to be useful for PH.
In some patients, PH can coexist with trigeminal neuralgia (PH-tic syndrome); similar to cluster-tic syndrome, each component of it may require separate treatment.
Secondary Paroxysmalhemicrania
Secondary PH has been reported with lesions situated  in the region of the sellaturcica, such as 
  • Arteriovenous malformation
  • Cavernous sinus meningioma
  • Epidermoid tumors.
Secondary PH is more likely if the patient requires high doses (>200 mg/d) of indomethacin.
In patients with apparent bilateral PH, raised CSF pressure should be suspected. One point to be kept in mind  is that indomethacin can reduces CSF pressure. When a diagnosis of PH is considered, MRI brain  is indicated to exclude a pituitary lesion.

What is primary sex headache?

Primary sex headache is precipitated by sexual excitement. 
The pain  usually starts as a dull bilateral headache that suddenly becomes intense at orgasm. 
The primary sex headache can be prevented by ceasing sexual activity before orgasm. 
There are three types of sex headache.
  • A dull ache in the head and neck that intensifies as sexual excitement increases
  • A sudden, severe, explosive headache occurring at orgasm
  • A postural headache developing after coitus that resembles the headache of low CSF pressure. The latter arises from vigorous sexual activity and this is a form of low CSF pressure headache.
Headaches occuring at the time of orgasm are not always benign

5–12% of cases of subarachnoid hemorrhage are precipitated by sexual intercourse. 
This type of headache is reported by men more often than women 
Sex headache  may occur at any time during the years of sexual activity.
This may develop on several occasions in succession and then not trouble the patient again, even without an obvious change in sexual activity. 
In patients who stop sexual activity when headache is first noticed, the pain may subside within a period of 5 min to 2 h.
In about fifty percentage of patients, sex headache will subside within 6 months.
About fifty percentage of patients with sex headache have a history of exertional headaches, but there is no excess of cough headache. 
Migraine is probably more common in those patients with sex headache
Benign sex headaches recur irregularly and infrequently.
Treatment of primary sex headache
  • Management can often be limited to reassurance and advice 
  • Propranolol can be used to prevent headache that recurs regularly or frequently, the dosage required varies from 40 to 200 mg/d. 
  • Other drug is calcium channel–blocking agent diltiazem, 60 mg tid. 
  • Ergotamine (1 mg) or indomethacin (25–50 mg) taken about 30–45 min prior to sexual activity can also reduce the headache.

How headache is produced?

Pain usually generated when peripheral nociceptors are stimulated in response to tissue injury, visceral distension, or other factors.In such situations, pain perception is a normal physiologic response mediated by a healthy nervous system.
Pain can also result when pain-producing pathways of the peripheral or central nervous system (CNS) are damaged or activated inappropriately.
Headache may originate from either or both mechanisms.
Relatively few cranial structures are pain-sensitive they are
  • Scalp
  • Middle meningeal artery
  • Dural sinuses
  • Falx cerebri
  • Proximal segments of the large pial arteries. 
Structures that are not painsensitive
  • The ventricular ependymal
  • Choroid plexus
  • Pial veins
  • Much of the brain parenchyma 

Warning signs in headache

Following are the warning signs in headache 

Worst headache ever 
First severe headache 
Subacute worsening over days or weeks 
Abnormal neurologic examination 
Fever or unexplained systemic signs 
Vomiting that precedes headache 
Pain induced by bending,lifting, cough
Pain that disturbs sleep or presents immediately upon awakening 
Known systemic illness
Onset after age 55
Pain associated with local tenderness, e.g.region of temporal artery