There are thousands of causes of headaches, and it is difficult for the director of this case to judge...

*Only for medical professionals to read and reference layer by layer analysis, temper clinical diagnosis and treatment thinking

In clinical work, we often encounter patients with headaches, take a report printed with the words "lacunar cerebral infarction or cerebral deficiency" and ask: Doctor, is my headache caused by this lesion? How do we, as doctors, answer this? Let's start with a case~

The main points of this example

First look at the case data

Combined with the case's medical history, physical examination, and adjunctive examination, the diagnosis is clear

The presence of tension headache and migraine is first suspected, and the diagnostic criteria for combining migraine and tension headache are currently not met and are less likely

After the patient was admitted to the hospital, we only gave standard cerebral infarction treatment, and did not give other analgesic treatments, and the patient's headache gradually eased

Therefore, the headache is more likely

Literature Query: How Does Cerebral Infarction Cause Headaches?

It is well known that some patients with cerebral infarction experience headaches, especially those with posterior circulation cerebral infarction, and according to relevant studies, about 9% to 25% of patients with headaches due to cerebral infarction [1].


However, there are currently no literature reports
on whether arteriolar occlusive cerebral infarction causes headache and headache mechanism.

Next, let's explore the mechanism of headache caused by cerebral infarction, which probably has the following reasons [2-4]:

(1) When ischemia and hypoxia occur in the local area, compensatory dilation of the surrounding collateral circulation vessels will occur, and pain
will appear in the relevant pain-sensitive structures in the skull.

(2) Pain
occurs when brain tissue containing trigeminal nerve endings is stimulated by ischemia and hypoxia.

(3) When the brain tissue ischemia and hypoxia occur, cytotoxic edema and angioedema occur in the tissues around the lesion, resulting in a rapid increase in intracranial pressure, and the large blood vessels and pia mater are pulled and squeezed, resulting in headaches
.

(4) Ischemic brain tissue activates platelet aggregation, releases oxygen radicals, bradykinin, serotonin and other analgesic substances, stimulates intracranial pain-sensitive structures and causes headache
.

(5) When brain tissue ischemia and hypoxia, the release of endorphins, enkephalins and other pain suppressant substances is reduced; The pain threshold is lowered and headache occurs
.

(6) When ischemia and hypoxia appear in the cerebral cortex, it is easy to affect the venous blood vessels, sinuses and capillaries on the surface of the brain, and the reason is that the hypoxic site is an important pain-causing tissue in the skull, which is easy to cause headaches
.

(7) When the compensatory collateral circulation of the era of large vascular occlusion is established, it causes significant dilation of intracranial and extracranial blood vessels or causes headaches
due to the traction of certain blood vessels.

(8) When there is ischemia and hypoxia in the vertebro-basilar artery system, its headache may be related
to the cerebellum, brainstem damage, edema exacerbation stimulation of the meninges, and stimulation of the trigeminal spinal tract nucleus of the myeloidoid lesion.

Arteriolar occlusive cerebral infarction refers to the smaller perforatum artery in the cerebral hemisphere or deep brainstem, on the basis of various diseases, the vascular wall lesions, resulting in narrowing of the lumen to occlusion, the formation of small infarction foci
.

When arteriolar occlusive cerebral infarction occurs in non-functional areas of the brain, patients generally do not have any clinical symptoms, and clinical symptoms such as limb weakness and numbness occur in functional areas
.

Combined with the pathogenesis of headache caused by cerebral infarction, the current mechanism of headache caused by arteriolar occlusive cerebral infarction is considered:

1.
Post-circulating ischemia and hypoxia stimulate the trigeminal nerve spinal tract nucleus causing headache;

2.
During the precirculation, ischemic and hypoxic tissue causes platelets to release oxygen free radicals, bradykinin, serotonin and other analgesic substances to increase, or ischemic and hypoxic brain tissue to release endorphins, enkephalins, amino acids and other pain suppressant substances
.

In summary, when encountering patients with arteriolar occlusive cerebral infarction and headache in clinical work, it is necessary to comprehensively consider the range of blood supply to brain tissue by the perforational artery and the location of the arteriolar occlusive cerebral infarction, and whether it is the cause of
the headache.

Therefore, in clinical work, when diagnosing headache caused by arteriolar occlusive cerebral infarction, it is necessary to comprehensively analyze
it.

References: [1] Vestergaard K,Andersen G,Nielsen MI,et al.
Headache in stroke.
[J].
Stroke,1993,24(11):1621-1624.
[2] Gossrau G,Dannenberg C,Reichmann H,et al.
[Thunderclap headache caused by cerebellar infarction].
[J].
Schmerz,2008,22(1):82.
[3] Mitsias P,Ramadan N M.
Headache in Ischemic Cerebrovascular Disease.
Part I:Clinical Features[J].
Cephalalgia,2010,12(5):269-274.
[4] Portenoy R K,Abissi C J,Lipton R B,et al.
Headache in cerebrovascular disease.
[J].
Stroke,2015,15(6):1009-1012.
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The source of this article Medical Neurology Channel Author | Deng Caihong reviewed this article | Li Tuming responsible
editor Mr.
Lu Li

Copyright notice
This article is original, reprint please contact the authorization-End-

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