A stroke after waking up?

*Only for medical professionals to read and refer to a case of "stroke after waking up?"
Wake-up stroke (WUS) is a research hotspot of ischemic cerebrovascular disease in recent years.

There is no clear definition of WUS, but most literature tends to classify as WUS the type of neurological deficit symptoms found after getting up without obvious abnormalities before going to bed.

Its prevalence varies from study to study, accounting for approximately 15%-30% of all stroke cases.

The case shared with you today is a bit different from the usual stroke after waking up.
Let’s take a look at its reversal plot.

Case introduction Patient Xia, male, 80 years old, was admitted to the hospital mainly because of "discovered unconsciousness for 1.
5 hours".

The patient watched TV at home at about 6:00 a.
m.
on August 21, 2020.
Everything was normal.
Then he went to the bedroom to rest.
At about 8:00 a.
m.
, the family members called the patient and did not respond.
The patient was found lying in bed, unconscious and breathing.
Deep and slow, limbs palsy, no fever or convulsions.

The family members rushed the patient to our hospital and arrived at the emergency department of our hospital at 8:40 in the morning.
After the emergency doctor performed first CT and other related examinations, they were admitted to the general ward of our hospital with "stroke after waking up?" at about 9:10.
The patient suffered spontaneous illness.
Since then, the mental state is poor, and he has incontinence without eating.

Smoking for more than 40 years, 1 pack/day.

A history of pulmonary heart disease for many years.

Physical examination: body temperature 36.
5℃, pulse 139 beats/min, breathing 30 beats/min, blood pressure 127/70 mmHg, weight 70kg.

He was in a shallow coma and was pushed into the ward on a flat car.
He was uncooperative on physical examination.
Breath sounds in both lungs were clear.
Damp rales could be heard in the bottom of the right lung.

The heart rate is 166 beats/min, the rhythm is irregular, the first heart sound varies in strength, and there is no murmur in the auscultation area of ​​each valve.

Nervous system examination: superficial coma, advanced cortical function examination can not be completed, cranial nerve: bilateral pupils are equal, D=2.
0mm, the right pupil is slow to reflect light, facial patterns are symmetrical, and the extra cranial nerve examination is not cooperative.

The muscle strength of the limbs cannot be measured.
According to the assessment of the patient's involuntary movement, the muscle strength of the left limb is 2-3, and the muscle strength of the right limb is 3-4.
The muscle tension test does not cooperate, the ataxia test cannot be completed, and the deep and shallow sensation , Complex physical examination is not cooperative, the right tendon reflex is active, the right pathological reflex is positive, the National Institutes of Health Stroke Scale (NIHSS) score is 27 points (consciousness level 3 points + questioning 2 points + instruction 2 points + limbs Muscle strength 12 points + sensation 2 points + language 2 points + articulation 2 points + neglect 2 points), Glasgow Coma Score (GCS) score of 5 points (1 point for eyes open + 1 point for speech + 3 points for limb flexion when stinging) ).

Auxiliary examination: head CT showed multiple cerebral infarction.

ECG and monitoring indicate atrial fibrillation.

The random blood glucose is 8.
0mmol/L.

Head CT before admission 1: Multiple lacunar cerebral infarction in both hemispheres and vertebrobasilar arteriosclerosis.

Subsequent blood tests, coagulation and biochemical returns: neutrophil percentage 76.
7%, lymphocyte percentage 18.
5%, average platelet volume 8.
8fL, high sensitivity C-reactive protein>5.
0mg/L, D-dimer 1.
79mg/L.

Myoglobin 25.
99ng/mL, creatine kinase isoenzyme <3.
00ng/mL, blood glucose 9.
09mmol/L, apolipoprotein A 1.
99g/L, apolipoprotein B 0.
54g/L, potassium ion 3.
29mmol/L , Sodium ion 135.
5mmol/L, homocysteine ​​19.
0umol/L.

Positioning and qualitative analysis: Positioning diagnosis: the patient's consciousness disorder, positioning the extensive cortex or brainstem ascending reticular activation system, the right pupil is slow to light reflection, positioning the light reflection pathway, the oculomotor nerve may be, and the limbs have involuntary movement , The right side is weak and the pathological signs on the right side are positive, the left pyramidal tract is located, and the brainstem is initially comprehensively located.

Qualitative diagnosis: the patient is elderly male, with acute onset, past history of pulmonary heart disease, long-term smoking history, ECG monitoring after admission indicates atrial fibrillation, there are multiple high-risk factors for cerebrovascular disease, head CT excludes bleeding and space occupation, first consider acute Ischemic cerebrovascular disease-basilar artery tip syndrome (TOBS), the mechanism of cardiogenic embolism may be possible, and secondly, the possibility of infection, poisoning, metabolic disorder, etc.
needs to be ruled out.

Diagnosis and treatment process: Due to the epidemic period, the patient was admitted to the transitional ward from the emergency department.
At 9:20 on August 20, 2020, the doctor in the transitional ward requested a neurology consultation, and asked about the past history and medication history.
There was no special diagnosis.
The initial diagnosis of acute cerebral infarction was performed.
Alteplase (rt-PA) was given intravenous thrombolysis at 9:25.
The patient weighed 70kg, calculated at 0.
9mg/kg, and the total amount of injection was 63mg.
The first dose was 6.
3mg intravenously, and the intravenous injection was completed within one hour.
.

One hour after thrombolysis, the patient's consciousness gradually cleared, speech was not clear, and advanced cortical function examination was slow, but it could be cooperated.
Cranial nerve examination: bilateral pupil diameters were 3.
0, reflexes returned to normal, and other cranial nerve examinations were normal.

Extremities muscle strength basically returned to normal, bilateral deep and superficial sensations, no abnormalities in compound sensory examination, normal abdominal wall reflex, active right tendon reflex, positive right pathological reflex, NIHSS score 2 points (level of consciousness questioning 1 point + articulation 1 point), GCS: 15 points, and Modified Rankin Scale (mRS): 1 point.

Three hours after thrombolysis, the patient was conscious, spoke fluently, answered relevant questions, cranial nerve examinations were normal, extremities muscle tone was normal, bilateral sensations of deep and shallow limbs, complex sensations were normal, and the right pathological reflex was positive.

NIHSS score 0 points, GCS: 15 points, mRS: 0 points.

2020-08-21 15:00 Figure 2: The reexamination of the head CT compared with the head CT at admission did not change.

On the second day after admission, the head MR image was re-examined.
Figure 3: DWI showed no new infarction, and no obvious stenosis of the large intracranial blood vessels.

Etiology retrospective: When the patient was admitted to the hospital, it was found that the pupils on both sides became smaller.
With doubts, the patient’s family members were asked whether they had a history of oral sleeping pills and psychotropic drugs.
The patient’s family members answered clearly that there was no.

Since the patient’s family is an endocrinologist in our hospital, it is as simple as possible to communicate about thrombolysis and take medication quickly.

On the second day after admission, when he asked the patient again, the patient complained that after waking up at about 6 a.
m.
that day, he quarreled with his wife.
After returning to the bedroom, the more he wanted to get angry, he immediately took out the clozapine tablets that his wife took orally.
Taking 50 mg orally, the cause of the disease will be revealed.

The patient's final diagnosis: stroke mimic (SM); clozapine poisoning.

Case discussion and analysis 1.
The definition of SM, common causes and coping >
Coping method: Once SM is identified, treatment should be based on the cause, but if there is a neurological deficit that cannot be distinguished from stroke in the emergency department, if the head MRI is not available, the doctor should actively give rt if it is within the time window.
-PA thrombolytic therapy, especially when posterior circulation stroke is suspected.

This patient is a relatively rare case of psychiatric drug abuse caused by SM.
It is clinically necessary for us to carefully screen out the questions and tendencies in the examination process when we are in the clinic.

2.
Evaluation of the safety of thrombolysis in patients with SM.
This patient has an acute onset and a history of pulmonary heart disease, but there is no high-risk cerebrovascular disease high-risk factors such as hypertension and diabetes.
Combined with the question of physical examination on admission , Once let the consulting doctor hesitate, but after admission, the ECG monitoring and ECG showed atrial fibrillation, we had to increase our vigilance, greatly increasing the possibility of posterior circulation stroke with embolic mechanism, and at the same time taking drugs that were initially suspected As a result of SM, the patient’s family gave a clear denial at the time, which led us to be more convinced of the diagnosis of acute ischemic stroke at first.
After active thrombolytic therapy, the patient’s symptoms gradually recovered, making clinicians more inclined to diagnose acute Ischemic stroke.

At present, there are only a few reports of symptomatic intracerebral hemorrhage (sICH) in SM patients after thrombolysis.
Most studies have not found cases of sICH and other serious complications after SM thrombolysis.

However, some scholars pointed out that in retrospective studies, for patients who have received thrombolytic therapy, doctors will tend to diagnose acute ischemic stroke, causing bias.

Especially for patients whose symptoms worsen due to complications after thrombolysis, it is more difficult for doctors to overturn the diagnosis of acute ischemic stroke.

Therefore, the risk of intracranial hemorrhage after SM thrombolysis in actual clinical work may be higher than these research data.

In the NINDS study, the incidence of small stroke sICH with NIHSS scores of 0-5 points was 2%.
It is speculated that patients with transient ischemic attack (TIA) and SM patients should have a lower risk of bleeding.

At present, there is still a lack of research data on the risk of intracranial hemorrhage in patients with migraine, epilepsy, etc.
after intravenous thrombolysis.

In patients with acute pulmonary embolism, no intracranial hemorrhage was found after thrombolysis, and the risk of intracranial hemorrhage after thrombolysis in patients with acute myocardial infarction was about 1%.

Some scholars speculate that the risk of intracranial hemorrhage after thrombolysis in SM patients who also have no intracranial ischemic injury should be comparable.

In 2013, a multi-center study conducted by Zinkstok et al.
included 5581 patients with thrombolytic therapy.
It is the largest study on the safety of SM thrombolytic therapy.

The risk of sICH in SM patients is 1.
0%, which is consistent with previous scholars' speculation.

A total of 100 cases of SM were diagnosed in the study.
According to the ECASS-II standard of symptomatic intracranial hemorrhage, 1 case of sICH (1%) occurred; and 2 cases of sICH (2%) occurred according to the NINDS standard.

Both cases were elderly male patients with epilepsy, and their prognosis was good for 3 months.

Regardless of whether the ECASS-II standard or the NINDS standard is used, the risk of sICH after SM thrombolysis is significantly lower than that of stroke patients.

3.
Clinical manifestations and treatment of clozapine poisoning.
Because clozapine has a definite effect on refractory schizophrenia, and there are few extrapyramidal reactions, it is favored by clinicians.

However, due to suicide, mistaking and other reasons, acute clozapine poisoning also occurs from time to time.

Clozapine has effects on multiple pathways such as monoamine transmitters, glutamatergic, gamma-aminobutyric acid, and cholinergic.
Therefore, the clinical manifestations of clozapine in acute poisoning are outstanding and abundant, and the poisoning can cause more System damage is mainly the nervous system, respiratory system, and cardiovascular system, and the mortality rate is about 10% to 12%.

According to the instructions of the drug instructions, oral absorption of clozapine tablets is fast and complete, and food has no effect on its absorption rate and degree.
After absorption, it is quickly and widely distributed to various tissues.
The bioavailability varies greatly from individual to individual, with an average of about 50% to 60% , There is a liver first pass effect.

The peak plasma concentration is reached 3.
2 hours (1 to 4 hours) after taking the drug, the elimination half-life (t1/2β) is an average of 9 hours (3.
6 to 14.
3 hours), the apparent volume of distribution (Vd) is 4.
04 to 13.
78L/kg, and the tissue binding rate is high.
.

It is metabolized by the liver, and 80% is present in urine and feces in the form of metabolites.
The main metabolites are N-desmethylclozapine and N-oxide of clozapine.

Treatment after poisoning is mainly to establish and maintain airway patency, induce vomiting and gastric lavage in time, and in addition to symptomatic and supportive treatment, hemoperfusion treatment should be performed as soon as conditions permit.
Colleagues who are actively treated should continue to monitor vital signs and organ functions to strive for better Good outcome.

The patient’s manifestations include coma, atrial fibrillation, and respiratory failure, which are consistent with the acute toxicity of clozapine tablets.

Since this patient was taking clozapine tablets for the first time, the dose was not large.
Although he was not given timely gastric lavage, catharsis, hemoperfusion and other treatments, it did not lead to serious consequences and the prognosis was good.

Reference materials: [1] Li Guangshuo, Bi Guorong.
Clinical features, imaging features and pathogenesis of stroke after awakening[J].
International Journal of Cerebrovascular Diseases, 2018, 26(11): 838-846.
[2] Zhang Yi, Han Yanfei, Dong Wei, et al.
Common stroke simulation diseases and their differentiation from emergency stroke[J].
Journal of Clinical Neurology, 2018, 31(6): 472-473.
[3] Wu Jian, Liu Chenyu, Ma Qingfeng .
Pay attention to the stroke simulation disease in intravenous thrombolysis[J].
Chinese Medical Journal, 2013, 93(43): 3412-3414.
[4] Sun Yaqi, Wang Ziyang, Wang Yumei (Hebei Medical University First Hospital, Hebei Medical University Spirit Institute of Health) Reading: Clozapine Poisoning | Clinical Essentials 2019-08-13 [5] Zinkstok SM, Engelter ST, Gensicke H.
, et al.
Safety of thrombolysis in stroke mimics: Results from a multicenter cohort study [J].
Stroke: A Journal of Cerebral Circulation, 2013, 44(4).