Intracranial "full of stars", the cause is...

*Only for medical professionals to read and refer to the Neurological Archives: layer by layer analysis to cultivate clinical thinking.

The cause of a disease may be common, unexpected, or uncommon; different regions have different dietary habits and different disease spectrums.

The diagnosis of the disease will change the entire treatment plan, and also allow patients to avoid unnecessary invasive examinations and additional costs.

Intracranial imaging "Gypsophila paniculata" refers to multiple focal lesions in the brain with obvious edema around it.
After injection of contrast medium, it shows ring-like or nodular enhancement, scattered and distributed.
It is common in brain metastases, cerebral cysticercosis, and tuberculous meninges.
In the case shared with you today, the cause is uncommon and related to eating habits.
It is easy to be misdiagnosed and mistreated.
How to make a correct diagnosis? The analysis by Tang Wei, director of the Department of Neurology, Xinhua Hospital Affiliated to Dalian University, is as follows: Case introduction female, 34 years old, from Yunnan Lahu ethnic group, was admitted to the hospital due to headache, vomiting for 20 days, and disturbance of consciousness for 2 days.

The patient had a headache 20 days ago, which was a persistent pain, a total headache, accompanied by vomiting, vomiting of stomach contents, non-jetting.

The symptomatic treatment did not improve.
Two days ago, the patient was unconscious and did not respond.
He came to the hospital for further diagnosis and treatment, and was admitted to the hospital with unconsciousness pending investigation.

Since the onset, the patient has had no fever, no convulsions, and incontinence.

Physical examination: heart rate 56 beats/min, thin body, severe malnutrition, weight 45 kg, light coma, and presence of orbital pressure reflex.

Occasionally restlessness, eyes staring to the left, both pupils 3.
0mm, sensitive light reflection.

Neck strength (+), Klinefelter sign is positive.

All limbs respond to pain irritation.

The bilateral pathological signs were negative.

The patient lives in a poverty-stricken area of ​​Yunnan, her husband is disabled, and the patient is the main labor force of the family.

Have a daughter.

Denies a history of drug exposure.

Have the habit of eating raw meat, and often eat raw pig blood and mixed raw pig skin (see Figure 1 below).

Figure 1: After admission to the hospital, a complete head CT of raw pig skin mixed with raw pig blood showed that there were flaky low-density shadows in the double frontal lobe, left occipital lobe, and bilateral basal ganglia, and the left occipital lobe lesions were larger (see Figure 2).

The blood cysticercosis antibody test is suspiciously positive.

Lumbar puncture cerebrospinal fluid cerebral pressure 180 mmH2O, protein 0.
82g/L, glucose 1.
94 mmol/L, chloride 106 mmol/L, cell number 43X106/L, and mononuclear cells accounted for 90%.

Head MRI showed that the lesions were mostly nodular, lumpy or patchy.
The T1WI sequence showed moderate to low signal, and the T2 pressure sequence showed high signal.
The brain parenchyma around the lesion was accompanied by different degrees of edema.

ADC phase dispersion is not limited (see Figure 4, Figure 5, Figure 6).

On enhanced MRI scan of the head, there are diffuse nodules and ring-shaped abnormal enhanced signal shadows in the lesion area of ​​varying sizes, and the "off-center target sign" can be seen.

The meninges also showed abnormal enhancement in strips and nodules (see Figure 7 and Figure 8).

Lung CT was normal.

There was no abnormality in the overall examination of the tumor.

Human immunodeficiency virus (HIV) antibody screening was negative, and the initial diagnosis was cerebral cysticercosis.
Bendazole was given orally.
During the deworming period, dimi 10mg and mannitol were treated once a day for 8 days.
The condition did not improve significantly.

Further head MRI reading, cerebrospinal fluid Toxoplasma IgG antibody (+) (see Figure 3), to correct the diagnosis.

Diagnosis: Cerebral toxoplasmosis.

Treatment: Sulfamethoxazole-trimethoprim (SMZ-TMP) 1.
44g/time, oral, 3 times/d; Azithromycin 0.
5g/d, intravenous injection, 1 time/d; methylprednisolone needle 80mg, daily One static point; 250ml of mannitol, static point every 8 hours.

Figure 2: Head CT shows that there are patchy low-density shadows in the double frontal lobe, left occipital lobe, and bilateral basal ganglia.
The left occipital lobe lesions are larger.
Figure 3: Cerebrospinal fluid Toxoplasma IgG antibody (+) Figure 4: T1WI sequence frontal lobe , Left occipital lobe, bilateral basal ganglia, and cerebellum can see sheet-like low signal and larger left occipital lobe lesions. Figure 5: The bilateral parietal lobes on the T2 water pressure sequence are mostly high signal, and the "eccentric target sign" can be seen in the bilateral basal ganglia, cerebellum, and left occipital lobe.

Low signal in the middle and high signal in the periphery.
The brain parenchyma around the lesion is accompanied by signals of different degrees of edema.

Figure 6: ADC-phase lesions are mostly iso-signal and high-signal, and the dispersion is not limited.

Figure 7: In the sagittal view of the enhanced head MRI scan, the frontal, parietal, occipital, cerebellum, and basal ganglia regions can be seen diffusely with different sizes of nodules and ring-shaped abnormal enhanced signal shadows, and the "off-center target sign" can be seen.

Figure 8: The axial position of the enhanced MRI scan of the head shows diffuse nodules and ring-shaped abnormal enhancement signal shadows of different sizes in the frontal, parietal, occipital, cerebellum, and basal ganglia areas, and the "off-center target sign" can be seen.

The meninges also showed abnormal enhancement in strips and nodules.

Discussion 1 The imaging characteristics and pathological changes of cerebral toxoplasmosis.
The common intracranial imaging manifestations of toxoplasmosis are multiple focal lesions with obvious surrounding edema.
After the injection of contrast medium, it shows ring-like or nodular enhancement.
The lesions are usually It is located at the cortex-medullary junction, basal ganglia and thalamus.
Other locations such as the brainstem and corpus callosum are rare.

The main features of brain MRI lesions are as follows: (1) The frontal lobe, basal ganglia and thalamus are the main lesions, while the ventricles and ventricular membranes are rarely infringed; (2) Multiple lesions are seen in the brain, and the shape of the lesions is similar Mainly round or nodular; (3) The signal of the lesion is mainly low signal on T1WI, and mostly high signal on T2WI; (4) The enhancement form of the lesion after enhancement mainly shows ring enhancement, petaloid and nodular enhancement (5) The "target sign" after MRI T1WI enhancement has certain diagnostic significance.
The "eccentric target sign" is a typical MR manifestation of toxoplasmosis, including 3 layers: the innermost enhanced core (eccentricity is more common), the middle It is a low-signal area, and the outermost layer is a high-signal enhancement ring.

The specificity is 95% and the sensitivity is 25%.

CT of the patient showed that there were flaky low-density shadows in the double frontal lobe, left occipital lobe, and bilateral basal ganglia, and the left occipital lobe lesions were larger.

Head MRI showed that the lesions were mostly nodular, mass or patchy, T1WI sequence showed moderate to low signal, and mostly high signal on the water phase of T2 pressure, showing "eccentric target sign", in the brain around the lesion Parenchymal with signals of varying degrees of edema.

The ADC phase diffusion limitation of the lesion is not obvious.

On enhanced scan, the lesion area can be seen with diffuse nodules and ring-shaped abnormal enhanced signal shadows of varying sizes, and "off-center target sign" can be seen.

The meninges were also abnormally strengthened in strips.

It accords with the imaging characteristics of cerebral toxoplasmosis.

Figure 9: 1.
The outer layer of high signal strengthening ring; 2.
The middle is the low signal area; 3.
The inner layer of strengthening core (eccentricity is more common) Toxoplasmosis can form acute or chronic inflammatory lesions in the brain.

For milder lesions, perivascular inflammation, cell infiltration, and glial cell hyperplasia can be seen.

The small focus enhancement seen by our head MRI enhancement is the hyperplastic nodule.

When the disease is severe, necrotic foci and infiltration of lymphocytes, plasma cells, and eosinophils can be seen in gray and white matter, and they form a granuloma-like structure with proliferating glial cells (eccentric target sign inner high-confidence zone) .

We can also see the so-called Toxoplasma abscess, that is, the center of the lesion is necrotic cell debris (the low signal area in the middle of the eccentric target sign), and the surrounding is edema and inflammatory brain tissue; vascular abnormalities, including lymphatics around the blood vessel and the blood vessel wall Cell infiltration (eccentric target sign outer high signal area); endothelial cell swelling, thrombosis, fibrinoid necrosis of the tube wall and luminal fibrosis occlusion.

The pathogen of Toxoplasma gondii can be seen in and around the necrotic foci of brain tissue.

Some scholars believe that the annular enhancement after enhancement is related to the inflammation changes and vascular proliferation surrounding the lesion.

And pointed out that the infiltration of macrophages in the blood vessel wall destroys the blood-brain barrier is the main reason for the enhancement.

2 The pathogenesis of cerebral toxoplasmosis Toxoplasma gondii is an obligate intracellular parasitic protozoan.
It has a wide host group and is prevalent worldwide.
Common susceptibility factors include close contact with domestic cats, eating raw or semi-raw meat, Close contact with soil, water and blood containing oocysts.

Patients often get infected by accidentally eating oocysts or being bitten by animals.

Residents in some areas (such as Yunnan) like to eat raw or semi-raw meat.
If there are surviving oocysts in the meat, infection may occur after ingestion.

This patient has a history of eating raw meat, which should be the cause of his infection with Toxoplasma gondii.

Studies have shown that infrequent cleaning of kitchen supplies after handling raw meat is associated with Toxoplasma infection.
Toxoplasma enters the human body by any means, and can invade the nucleated cells of various tissues and organs directly or through lymph and blood.
It can enter the cell through the phagocytosis of phagocytes.

Tachyzoites are the main pathogenic stage and are antigenic.

Humans lack innate immunity to Toxoplasma gondii.

In the early stage of infection, the tachyzoites of Toxoplasma gondii rapidly multiply in nucleated cells and form pseudo-cysts; when the cell structure is destroyed, the tachyzoites are released from the cell and invade adjacent cells again, and so on.

Acquired infections in healthy adults are mostly asymptomatic.

When the host's immune system is suppressed or the immune system is compromised, the worms in the body are activated and disseminated infection occurs, which aggravates the disease and even causes death.

Therefore, the occurrence and development of the disease are closely related to the virulence of the strain and the immune status of the body.

The patient in this case lives in a poverty-stricken area in Yunnan.
Her husband is disabled.
The patient is the main labor force of the family.

He has a weak physique, has a daughter, has a poor nutritional status, has a low immunity, and has a history of eating raw meat, causing disease.

Figure 10: Pathogenesis of Toxoplasma gondii 3 Gypsophila imaging differential diagnosis (1) Tuberculous meningitis: enhanced small ring enhancements are similar in size, scattered and distributed, moderate edema, and involving the brainstem, the distribution of lesions is based on the skull base area Mainly, it is the "white target sign.
"
(2) Brain metastases: metastases can be distributed in any part of the brain.
Because they are mainly spread through arteries, tumor thrombi tend to stay at the end of arteries (especially the middle cerebral artery), so supratentorial (5/6) brain metastases Tumors are more common than those under the curtain (1/6).

The forehead, parietal and temporal lobes are more common in the supratentorial area, accounting for more than 70%, and the cerebellar hemisphere is more common in the subtentorial area.

Other rare parts include the basal ganglia, hypothalamus, pituitary gland, brainstem, choroid plexus, pineal gland, fourth ventricle, semilunar ganglia, optic or olfactory nerves, etc.
, which are "black target signs" and are caused by tumorous lesions.

The main problem is the basal ganglia, which is not consistent with it.

(3) Cerebral cysticercosis: In general, cysticercosis are mostly distributed at the junction of gray matter and white matter in the brain, but their distribution in the gray matter nucleus is a relatively characteristic imaging manifestation.
It involves more gray matter nuclei and cortex in the basal segment.
The lesion has a complete ring shape, which is a "white target sign".

(See Figure 3) Figure 11: The images shown above are tuberculous meningitis, brain metastases, and cerebral cysticercosis in order.
4 Clinical manifestations and diagnosis of cerebral toxoplasmosis.
Cerebral toxoplasmosis has acute or subacute onset, and acute brain damage shows Diffuse and subacute cases are mostly focal brain damage, and then gradually develop to diffuse brain damage.

According to the location of the lesion, it can be divided into ventricular type, brain parenchymal type and mixed type.

The ventricular type is mainly manifested by intracranial hypertension and meningeal irritation; the brain parenchymal type may present symptoms such as epilepsy, intracranial hypertension, mental changes, sensory motor disorders, aphasia, and brain nerve damage.

The basis for clinical diagnosis includes: (1) Acquired immunodeficiency (AIDS) patients with severe immunodeficiency and those with weakened immunity caused by other reasons; (2) Clinical symptoms and signs: headache, fever, and focal Nervous system abnormalities, seizures, mental disorders, behavioral changes, ataxia, cranial nerve palsy, visual abnormalities, etc.
; (3) Laboratory examination: anti-Toxoplasma IgG antibody is positive, and cerebrospinal fluid examination shows lymphocytes mainly white blood cells Increased height, accompanied by increased eosinophils and protein; (4) Imaging examination: CT or MRI of the head can show clear circular enhancement with or without peripheral edema; (5) Exclude intracranial lesions caused by other pathogen infections or diseases ; (6) The anti-toxoplasma treatment is effective.

The patient has a subacute onset, a history of eating raw meat, malnutrition, headache, vomiting, and disturbance of consciousness.

The cerebrospinal fluid was positive for anti-Toxoplasma IgG antibody, and the head CT or MRI showed clear circular enhancement and eccentric target sign.
The current treatment is 3 days, and there is no obvious effect.

5 Treatment and prognosis of cerebral toxoplasmosis The course of anti-toxoplasma treatment is at least 6 weeks.

If the diagnosis is clear and the imaging performance is not improved significantly after 6 weeks of treatment, the course of treatment can be extended appropriately.

(1) Recommended program: sulfamethoxazole-trimethoprim (SMZ-TMP) (1.
44g/time, oral, 3 times/d) combined with clindamycin (600mg/time, intravenous injection, once every 6h ) Or azithromycin (0.
5g/d, intravenous injection, 1 time/d).

(2) Recommended program: Trimethoprim tablets (1.
44g/time, orally, once every 8h) combined with clindamycin or azithromycin.

(3) Recommended program: Clindamycin combined with Azithromycin: This program can be used when the patient is intolerant to sulfa drugs and pyrimethamine.

▌ Adjuvant therapy (1) Glucocorticoids: Hormone adjuvant therapy should only be used for patients with local brain disease or edema-related mass effect.

(2) Anti-epileptic drugs: Authors of epileptic seizures should give anti-epileptic treatment.

(3) Lower intracranial pressure: Patients with high intracranial pressure can use dehydrating agents such as mannitol for symptomatic treatment.