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Neurology Chapter 9 Other Diseases of the Nervous System
This is a mind map about Chapter 9 of Neurology and other diseases of the nervous system, which summarizes central nervous system infections, intracranial space-occupying lesions, etc.
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Neurology Chapter 9 Other Diseases of the Nervous System
- One Hundred Years of Solitude Character Relationship Chart
One Hundred Years of Solitude is the masterpiece of Gabriel Garcia Marquez. Reading this book begins with making sense of the characters' relationships, which are centered on the Buendía family and tells the story of the family's prosperity and decline, internal relationships and political struggles, self-mixing and rebirth over the course of a hundred years.
- One Hundred Years of Solitude Character Relationship Chart
One Hundred Years of Solitude is the masterpiece of Gabriel Garcia Marquez. Reading this book begins with making sense of the characters' relationships, which are centered on the Buendía family and tells the story of the family's prosperity and decline, internal relationships and political struggles, self-mixing and rebirth over the course of a hundred years.
- Project Management Process Template
Project management is the process of applying specialized knowledge, skills, tools, and methods to project activities so that the project can achieve or exceed the set needs and expectations within the constraints of limited resources. This diagram provides a comprehensive overview of the 8 components of the project management process and can be used as a generic template for direct application.
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- Outline
Neurology Chapter 9 Other Diseases of the Nervous System
Section 1 Central Nervous System Infection
I. Overview
【Classification】
[Route of infection] ① Blood-borne infection; ② Direct infection; ③ Retrograde infection of the nerve trunk (such as HSV, poliovirus, rabies virus)
2. Herpes simplex encephalitis (HSE)/acute necrotizing encephalitis
[Definition] It is an acute infectious disease of the central nervous system caused by HSV infection. It is the most common viral infectious disease of the central nervous system; it most commonly invades the temporal lobe, frontal lobe and limbic system, causing hemorrhagic necrosis of brain tissue and allergic reactions. sexual harm
[Pathogenesis] HSV-Ⅰ is mainly latent in the trigeminal ganglion, and HSV-Ⅱ is mainly latent in the sacral ganglion; adult HSV-Ⅰ encephalitis is mostly caused by reactivation of latent virus infection, accounting for the vast majority; HSV-Ⅱ encephalitis is Mostly primary infection
[Pathology] Brain parenchymal hemorrhage and necrosis; eosinophilic inclusions can be seen in nerve cells and glial cells, and the inclusions contain herpes virus particles and antigens (the most characteristic pathological change)
[Clinical manifestations] Sporadic, no seasonal difference; more common in adults, may have prodromal symptoms (such as fever, general malaise, headache, myalgia, drowsiness, abdominal pain, diarrhea); mostly acute onset, about 1/4 of patients have History of oral herpes; clinical manifestations include fever, headache, vomiting, mild disturbance of consciousness and personality changes, memory loss, hemiparesis, hemianopia, aphasia, ataxia, hyperactivity, and meningeal irritation. About 1/3 of patients may develop systemic symptoms. Sexual/partial epileptic seizures, some may first seek psychiatric treatment due to abnormal mental behavior; the condition progresses rapidly within a few days, manifesting as disturbance of consciousness, and in severe cases, intracranial hypertension and cerebral herniation may occur
【Auxiliary inspection】
laboratory
Routine blood test: visible WBC mild↑
Cerebrospinal fluid routine: normal/mild pressure↑, nucleated cell count↑ (mainly lymphocytes), protein mild to moderate↑, sugar/chloride normal
Cerebrospinal fluid etiology: detection of HSV-specific antibodies, HSV-DNA
Videography
CT: Focal abnormalities (low-density lesions in the frontotemporal region on one/both sides); however, there may be no abnormal findings on CT within the first 4 to 5 days after the onset of HSE symptoms.
MRI: early diagnosis, showing diseased areas
other
EEG: Diffuse high-amplitude slow waves (especially in the frontotemporal region)
Brain biopsy: the gold standard for diagnosis
[Diagnosis] Acute onset of high fever, accompanied by abnormal mental behavior, epileptic seizures, disturbance of consciousness or symptoms of brain parenchymal damage. The condition progresses rapidly. The cerebrospinal fluid shows viral encephalitis mainly composed of lymphocytes, and the intracranial pressure is significantly increased. It should be treated Consider the diagnosis of this disease
[Treatment] Antiviral treatment (acyclovir, ganciclovir), immunotherapy (interferon, transfer factor), glucocorticoids, antibacterial treatment, symptomatic supportive treatment (such as nutritional support, anti-epileptic/convulsive, cranial degeneration) pressure)
3. Introduction to other central nervous system infections
(1) Tuberculous meningitis
[Clinical manifestations] Subacute/chronic onset, with a small history of previous tuberculosis infection (20%); there may be no neurological manifestations in the early stage of infection, and headache and meningeal irritation gradually appear. Intracranial hypertension is common, accompanied by mental symptoms and confusion. , focal neurological deficit occurs in the later stage; the most common cranial nerve palsy is the abducens nerve, followed by the oculomotor nerve, trochlear nerve, and facial nerve; clinically, this disease is most easily confused with cryptococcal meningitis
[Examination] Cerebrospinal fluid examination: The pressure is obvious, and a film can be formed after being left alone; the number of cells is ↑ (mainly lymphocytes), sugar and chloride are obvious, and protein is ↑; Mycobacterium tuberculosis culture can be positive (gold standard for diagnosis)
(2) Neurosyphilis
[Clinical manifestations] All are late-stage syphilis; asymptomatic, meningitis and cerebrovascular disease are the most common
Asymptomatic type
Headache, dizziness, amnesia, difficulty concentrating, and poor sleep; most turn into symptomatic neurosyphilis
symptomatic
Meningeal vascular type
Meningitis type
Acute: acute onset of fever, headache, nausea, and meningeal irritation, similar to acute viral meningitis
Chronic: similar to tuberculous meningitis
Cerebrovascular disease type: acute stroke-like onset, mainly involving MCA
parenchymal type
∎ Paralytic dementia: amnesia, memory loss, cognitive function decline, and inability to take care of themselves; progresses rapidly, and severe dementia may occur within a few months; most intelligence can be significantly improved after treatment with Jingqi Mei
Tuberculosis spinal cord: Mainly affects the posterior cord and posterior roots; manifests as lightning-like pain in both lower limbs, difficulty walking in the dark, deep sensory loss in both lower limbs, sensory ataxia, and loss of knee/ankle reflexes in both lower limbs; some may have A -Rat pupils, 10~15% have visceral crisis (such as gastric crisis, intestinal crisis, urinary crisis)
[Examination] Cerebrospinal fluid examination: white blood cell count (mainly lymphocytes; at least 5×106/L in untreated patients), protein, sugar and chloride are normal; cerebrospinal fluid and blood syphilis tests are both positive
[Treatment] Treatment for dispelling plum blossoms: first take oral prednisone (to reduce Yahweh reaction), add daily intravenous infusion of penicillin from the 2nd day, and then intramuscular injection of benzathine penicillin
(3) Neurocysticercosis
[Clinical manifestations] Divided into epilepsy type, meningitis type, increased intracranial pressure type (Bruns syndrome may occur), dementia type, spinal cord type, and extracerebral manifestations (such as skin and muscle cysticercosis)
(4) Creutzfeldt-Jacob disease/CJD/cortical-striatal-spongiform degeneration/subacute spongiform encephalopathy
[Cause] It is caused by mutation of glycoprotein on normal cell membrane, PrPc → PrPsc; MM1 and MV1 types are the most common
[Pathology] Different degrees of symmetrical hemispheric atrophy can be seen grossly, and microscopically: ① cavernous degeneration (especially gray matter); ② loss of nerve cells (especially occipital lobe); ③ gliosis; ④ white matter fiber myelin Degeneration; ⑤Amyloid plaque (cerebellar molecular layer)
[Diagnosis] ① Progressive dementia for 2 years; ② Myoclonus, visual impairment, cerebellar symptoms, and akinetic mutism; ③EEG shows diffuse 0.5~2s periodic sharp-slow complex; ④14-3- can be found in cerebrospinal fluid 3 Protein positive; ⑤ Brain tissue biopsy shows spongiform degeneration and PrPsc positive (the most reliable basis for diagnosis)
Section 2 Intracranial space-occupying lesions
[Definition] Symptoms and signs caused by changes in the proportion of brain tissue, meninges, bone structures, and blood components in the cranial cavity occupying the volume of the cranial cavity; among them, intracranial tumors (the most common) and intracranial hematoma are the most common.
1. Increased intracranial pressure
[Cause and pathogenesis]
Cause
Increased volume of the brain tissue itself (cerebral edema → vasogenic, cytotoxic, mixed), increased cerebral blood flow, excessive cerebrospinal fluid, intracranial space-occupying lesions, and narrow cranial cavity
installment
Compensation stage (8~10% compensation volume) → early stage (non-localizing symptoms, Cushing reaction) → peak stage (scattered infarcts in the brain, signs of herniation, scattered Cushing reaction) → late stage (depletion stage)
[Clinical manifestations]
clinical manifestations
General symptoms (non-localized symptoms): three main signs of increased intracranial pressure - headache, vomiting, and papilledema
secondary symptoms
Visual loss and optic atrophy
Cerebral herniation: refers to a serious clinical phenomenon caused by continued increase in intracranial pressure, pressure, displacement and embedding of brain tissue; clinical manifestations include compression of the herniation itself/structure at the herniation site, blood circulation/cerebrospinal fluid circulation Various symptoms of obstruction, often leading to disturbance of consciousness and respiratory and circulatory arrest
Hiatal hernia of the tentorium/temporal uncus herniation: When supratentorial space-occupying lesions cause local increase in intracranial pressure, the uncus, hippocampal gyrus, lingual gyrus, etc. of the temporal lobe are displaced downward through the tentorial hiatus and cause compression. Midbrain (cerebral peduncle), great cerebral vein, oculomotor nerve; manifested as oculomotor nerve palsy on the affected side (pupil dilation, loss of light reflex, eyeball abduction, ptosis), incomplete central paralysis of the contralateral limb, and consciousness Obstacle; further displacement may cause damage to the oculomotor nerve nucleus on the affected side and central paralysis of the ipsilateral limb; in severe cases, foramen magnum hernia may result
Foramen magnum hernia: The posterior cranial fossa/supratentorial space-occupying lesion pushes the brainstem downward, and the cerebellar tonsils on both sides, adjacent cerebellar tissue, and medulla oblongata herniate downward into the spinal canal through the foramen magnum; manifested as neck pain and stiffness, The cranial nerve nuclei of the latter group are damaged (bradycardia, increased blood pressure, slowed breathing, vomiting, difficulty swallowing), but the consciousness is still clear and there are few pupil changes; at this time, if there is a sudden increase/fluctuation in intracranial pressure ( Such as severe coughing, vomiting, exertion, lumbar puncture, neck compression test), which can lead to respiratory arrest, coma, circulatory failure and death.
Secondary brain injury
Brainstem: Small hemorrhage/infarction near the midline of the tegmentum of the midbrain, especially the "pyriform brainstem" caused by bilateral tentorial hiatal herniation.
Reversible posterior cerebral leukoencephalopathy: caused by ischemic necrosis of the occipital lobe due to compression of the posterior cerebral artery at the free edge of the tentorium cerebelli.
Cerebral visceral syndrome: Increased intracranial pressure can cause acute pulmonary edema, peptic ulcer, cardiac arrhythmia, and liver and renal insufficiency.
Focal symptoms (localizing symptoms): focal epilepsy/symptomatic epilepsy, paralysis (especially upper motor neuron paralysis of one limb), visual disturbances, psychiatric symptoms
Presumptive localization symptoms
Definition: refers to symptoms caused by intracranial space-occupying lesions, increased intracranial pressure, and displacement of intracranial structures, which are not directly related to the space-occupying lesions themselves.
Type
Abducent nerve palsy: the most common; but abducens nerve palsy on one side has localization value (ipsilateral temporal lobe lesions)
Ipsilateral limb paralysis: more common in cerebellopontine angle lesions
other
Cushing reaction/systemic vasopressor reflex: acute increase in intracranial pressure causes blood pressure↑, heart rate↓, and respiratory slowdown; physiological significance: can increase cerebral perfusion, increase blood oxygen content, and improve cerebral hypoxia
Macewen Sign: Broken Can Sound
[Treatment] ① Control of increased intracranial pressure: head elevation, hyperventilation, osmotic agents, intracerebral catheter drainage, hypothermia treatment, etc.; ② Treatment of space-occupying lesions (treatment of the cause)
2. Intracranial tumors
[Clinical manifestations]
Features
Symptoms gradually worsen and neurological signs are superimposed
non-localized symptoms
Headache, vomiting, papilledema
Locate symptoms
Cerebral cortex: slightly
corpus callosum
Anterior part: progressive dementia, apraxia, personality changes
Middle part: Bilateral motor/sensory impairment, lower limbs heavier than upper limbs
Posterior: Parinaud syndrome, hydrocephalus
ventricular system
Third ventricle: intermittent increase in intracranial pressure, symptoms can be relieved automatically by changing body position; those who invade the front of the third ventricle may have symptoms of hypothalamic damage, and those who invade the rear may have Parinaud syndrome
Lateral ventricle: increased intracranial pressure, cerebrospinal fluid protein↑
Fourth ventricle: Early dizziness and vomiting, changes in head position can cause tumors to block the ventricular outlet, causing acute increase in intracranial pressure (Bruns syndrome); persistent obstruction of the ventricular outlet can cause hydrocephalus
Thalamus: Symptoms are relatively subtle, most of them only have headaches; mental symptoms, obesity, and polyuria may be present
Basal ganglia: sensory impairment, hemiparesis, involuntary movements, ataxia, nystagmus
Brainstem: Different levels can produce different localization symptoms
cerebellum
Hemisphere: Impaired coordination of limbs on the affected side, unclear speech, nystagmus, obvious muscle tension, and loss of tendon reflexes; staggering gait, prone to falling to the affected side
Vermis: Unsteady gait (duck gait), gradually develops into inability to walk, and falls backward when standing; however, the disorder of limb coordination and movement is often not obvious; it can easily cause obstruction of the fourth ventricle
Cerebellopontine angle: vertigo, tinnitus, progressive hearing loss, nystagmus, cerebellar signs
Intrasellar/suprasellar: early typical manifestations are endocrine disorders; after enlargement, there may be temporal hemianopia in both eyes.
Parasellar/clival: early typical manifestation is unilateral cranial nerve palsy (especially V and VI cranial nerves)
3. Brain abscess
[Clinical manifestations]
Features
It is more common in children and adolescents; early symptoms include fever, chills, headache, general weakness, drowsiness and fatigue, with further symptoms of focal nerve localization and intracranial hypertension appearing 1 to 2 weeks later.
type
Acute fulminant type: sudden onset, early coma, and high mortality; severe diffuse suppurative encephalitis can be seen at autopsy, and the abscess capsule may not be formed or may be partially formed.
Meningitis type: Mainly purulent meningitis (because the superficial location of the abscess causes severe inflammation in the adjacent subarachnoid space, masking the symptoms of the brain abscess itself)
Brain tumor type: The brain abscess capsule is intact, the surrounding edema has subsided, and the disease develops slowly
Hybrid
Occult type: There is no clear history of infection, surgical treatment is only performed because of intracranial space-occupying lesions, and the diagnosis is only made during the operation.
4. Pseudotumor cerebri/benign intracranial hypertension syndrome
[Characteristics] It is a group of diseases of unknown cause (now confirmed to be caused by venous sinus thrombosis) characterized by increased intracranial pressure, no focal signs of the nervous system, normal cerebrospinal fluid composition, and good prognosis; its diagnosis should be ruled out sexual diagnosis
5. Hydrocephalus
【Cause】
non-traffic
The lesion is located in or near the ventricular system, causing obstruction of the ventricles and inability to communicate with the subarachnoid space.
Transportation
The ventricles and subarachnoid space remain patent
[Clinical manifestations]
congenital
More common in congenital aqueduct occlusion
Acquired nature
Mainly manifested by increased intracranial pressure
Normal pressure hydrocephalus: progressive dementia without signs of increased intracranial pressure, difficulty starting, urinary incontinence