Middle-aged man continues to be dizzy and blurred vision, this case is very classic

*Only for medical professionals' reference to read the "big trouble" caused by "small points" clinically, most of the brainstem syndromes we encounter are atypical brainstem syndromes, once we encounter a typical brainstem syndrome Instead, I’m a little uncomfortable.
Today I’m sharing with you a rare but very typical brainstem syndrome.
Let’s take a look at how much trouble this “small” lesion has caused? Case introduction: Patient Jiang Mou, male, 58 years old.

Mainly due to "dizziness and blurred vision for 8 hours", he was admitted to our hospital on February 22, 2021.

The patient woke up at around 6 o'clock on February 22, 2021, and developed dizziness, blurred vision, and double shadow symptoms without obvious triggers.
When looking to the left side, dizziness is persistent, and it is related to opening eyes and closing eyes.
Dizziness can be reduced afterwards.

During the course of the illness, the symptoms of skewed mouth, nausea, and vomiting, no headache, fever, tinnitus, no physical sensation and abnormal activities, no speech disadvantage, hoarseness, drinking water, coughing, etc.
, unconscious disorder and feces disorder.

A history of lacunar cerebral infarction for 4 years, a history of hypertension for 1 year, irregular oral medications on weekdays, a history of smoking for many years, 1 packet a day, after left ear trauma.

Admission physical examination: blood pressure 181/96mmHg, clear consciousness, fluent speech, no abnormalities in cardiopulmonary and abdominal examinations, general examination of the nervous system: no abnormalities in high-level cortical function, cranial nerves: double pupils, equal circles, diameter 3mm, light reflection Sensitive, the left eyeball is fixed in the median position, adduction and abduction are limited, right eye adduction is limited, the right eye abduction position shows continuous horizontal rotation nystagmus, double vision, left frontal lines and nasolabial folds become shallow, The left eyelid has a weak closing force, and the left corner of the mouth is drooping, indicating that the mouth corner is deviated to the right.

Bilateral limb muscle strength is level 5, extremities muscle tension is normal, mutual aid examination is normal, bilateral limb tendon reflexes are symmetrical, bilateral limb deep and superficial sensations are consistent and symmetrical, bilateral pathological signs are positive, neck is not resistant, and meningeal irritation signs are negative.

The National Institutes of Health Stroke Scale (NIHSS) score is 4 points (gaze 2 points + left facial paralysis 2 points).

Video 1: The patient’s left eyeball cannot be adducted or abducted, and the right eyeball can only be abducted, not adducted, and peripheral facial paralysis on the left side (provided by the author, with the patient’s consent) Admission auxiliary examination: chest CT shows that the left lung is considered Localized emphysema in the lower lobe.

Head CT showed multiple lacunar infarctions in the basal ganglia on both sides.

The electrocardiogram shows T wave changes.

There were no abnormalities in blood routine, urine routine, and whole blood coagulation.

Total cholesterol is 6.
42mmol/L, low-density lipoprotein is 3.
74mmol/L, and small and dense low-density lipoprotein is 1.
61mmol/L.

 Positioning, qualitative diagnosis? Location diagnosis: The left eyeball of the patient can neither be adducted nor abducted, positioning the oculomotor nerve and abducens nerve, and the right eyeball abduction can not be adducted, positioning the oculomotor nerve.

For peripheral facial paralysis on the left, locate the left facial nucleus or peripheral nerves below it.

Integrated positioning of the pons, blood vessels positioning the basilar artery system.

Qualitative diagnosis: middle-aged male patient, acute and sudden onset, a history of long-term smoking, combined with a history of hypertension, hypercholesterolemia, and cerebral infarction, there are multiple high-risk factors for cerebrovascular disease, combined with the patient’s head CT without hemorrhage and occupancy First, consider acute ischemic cerebrovascular disease, and it is necessary to rule out multiple sclerosis, intracranial infection, inflammation and other possibilities.

Head MRI+MRA on February 23, 2021, the results are as follows: Figure 1: Head MR: DWI high signal on the left pontine cover, low signal on ADC lesions, multiple intracranial arteriosclerosis.

Clinically confirmed diagnosis: acute pontine infarction (eight and a half syndrome); hypertension grade 3 high-risk group; hypercholesterolemia.

Treatment process: After admission, he was given double antibodies for one week, and changed to monoclonal antibodies to smoothly lower blood pressure, strengthen lipid lowering, establish collateral circulation, and nourish nerves.

On the third day after admission, he started to cooperate with acupuncture and moxibustion treatment.
After 10 days of hospitalization, the patient was discharged.
At discharge, the dizziness basically disappeared.
The right eyeball was fully active than before, the left eyeball was still in the middle fixed position, and the peripheral facial paralysis on the left was slightly improved.

Instruct the patient to regularly take secondary preventive medication, continue acupuncture and moxibustion, and follow up.

Discussion Since eight and a half syndromes have been diagnosed, we have to go back to the source.
Let’s first understand what a one-and-a-half syndrome is.
The "one-and-a-half syndrome" (one-and-a-half syndrome) was first developed by Fisher in 1967.
It is proposed and reported that the lesions of one side of the pontine cover area not only invade the parapontine reticular formation (PPRF) lateral visual center or the abducens nucleus, but also involve the crossover of the contralateral contact ipsilateral eye movement Median longitudinal fasiculus (MLF) of the medial rectus nucleus; when the eyes look to the side of the lesion, the ipsilateral eye cannot be abducted, and the opposite eye cannot be adducted (gaze palsy); when the eyes look to the opposite side of the lesion , The ipsilateral eyeball cannot be adducted, but the contralateral eyeball can be abducted (internuclear ophthalmoplegia), and the abduction is often accompanied by horizontal nystagmus [1].

After understanding the one-and-a-half syndrome, plus the seventh pair of cranial nerve damage on the ipsilateral side, it is our current case "eight-and-a-half syndrome" [2], 1998, Eggenberger first proposed this syndrome.
Its anatomical basis is that the parapontine reticular structure (PPRF) and the medial longitudinal fascia (MLF) adjacent to the facial nerve are involved in the knee and facial nerve nucleus.

The mechanism of facial nerve palsy is not only caused by damage to the ipsilateral nucleus or fascicle (inner knee of the facial nerve) due to lesions of the pontine cover, it may also be caused by damage to the cortical medulla tract that connects the central anterior gyrus with the facial nerve nucleus.

The differential diagnosis of the eight and a half syndromes mainly includes cerebral hemorrhage, multiple sclerosis, intracranial tumor, inflammatory reaction, trauma, etc.
According to the patient's medical history, laboratory tests, and imaging examination results, the appealed diseases are basically excluded. Summary: This patient, a middle-aged male, has an acute onset, has hypertension, a history of cerebral infarction, has a blood pressure of 181/96mmHg at admission, has previously taken irregular antihypertensive drugs, has poor blood pressure control, has a history of cerebral infarction, and has no sequelae.
Irregular oral secondary preventive medications, long-term smoking in the past, the patient’s biochemical report after admission this time suggests hypercholesterolemia, there are multiple high-risk factors for cerebrovascular disease, combined with the pre-hospital examination and the patient’s head MR report after admission, the diagnosis is clear and acute Pontine infarction, the damage site is on the left pons covered part, the dot-like DWI high signal in front of the fourth ventricle, ADC low signal focus, once again let us see the characteristics of "small focus" and "big trouble" of brainstem infarction, this case The patient meets the clinical manifestations of the eight-and-a-half syndrome.

I am very grateful to Wang Yan from Hunan Brain Hospital for an article, "One and a half Syndrome Family".

Let us have a clearer understanding of the syndrome family derived from the "one and a half syndrome", especially the blue and white porcelain of Jay Chou that is still fresh in my memory [5].

"The sky is waiting for the rain, and I am waiting for you", I stand in place (the eyeball on the side of the lesion cannot be adducted or abducted), but you have to stay away (the eyeball on the opposite side of the lesion, deviating from the direction of the eyeball, can only be abducted, not inside Received).

Reference materials: [1]Shen Nei Xiaoliang, Turnip Discourse 3: One and a half syndrome 2017-08-08.
[2]Eggenberger Eric.
Eight-and-a-Half Syndrome[J].
1998.
[3]Li Xiaoxuan, Ren Yanyan , An Jin, Li Meixi, Wang Jianhua, Lu Peiyuan.
A case of pontine infarction with eight and a half syndromes[J].
Chinese Journal of Neuroimmunology and Neurology, 2017, 24(5): 374-375.
[4] Mestina BVQ , Sosuan GMN, Reyes KB.
Eight-and-a-half syndrome: a rare potentially life-threatening disease.
GMS Ophthalmol Cases, 2018, 8: Doc 4.
[5] Wang Yan, a half syndrome family-neurology record book 2019-04-13.