Progressive focal deficits General signs related to increased intracranial pressure

Neuro II (a) Flashcards by Elyaa Saleh

cause of Epidural Abscess

Direct local spread from an adjacent focus of infection (e.g. sinusitis, osteomyelitis, etc.)

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CF of Epidural Abcesses

Fever, headache and neck stiffness,
but also a variety of neurologic signs, lethargy and
coma if left untreated

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Progression and Complications of Epidural Abscess: Extension to the ———– -> ————- –> Mass effect –> ————- of the bridging veins –> Venous occlusion –> Brain Infarction

Extension to the subdural space -> Subdural Empyema –> Mass effect –> Thrombophlebitis of the bridging veins –> Venous occlusion –> Brain Infarction

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Epidural Absces –> ————

Subdural Empyema

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The 3 forms of Infectious Meningitis

1) Acute pyogenic (bacterial)
2) Aseptic (viral)
3) Chronic (Tbc)

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cause of Acute Pyogenic Meningitis in neonants

E. coli, group B Streptococci

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Cause of Acute Meningitis in adolescents and young adults

Neisseria meningitidis

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Cause of Acute Meningitis in older individuals

Streptococcus pneumoniae and Listeria monocytogenes

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CF of Acute Pyogenic Meningitis

1) Positive Kernig’s and Brudzinki signs
2) Neck stiffness
3) Vomiting
4) headache
5) Photophobia
6) Clouding of Consciousness
7) Irritablity

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Lab findings of Acute Pyogenic Meningitis

CSF examination:
* Abundant neutrophils
* Elevated protein
* Reduced glucose

Lumbar puncture: Increased pressure

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Macroscopic Features:
* Leptomeningeal exudate, over the surface
of the brain
* Engorged and prominent meningeal vessels

Microscopic Findings:
* Neutrophil cell infiltrates within subarachnoid
space
* Phlebitis and a thrombus
* Gram stain –> Pneumococcus meningitis- purulent exudate

featurse of?

Acute Pyogenic Meningitis

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Complications of Acute Pyogenic Mengitis

1) Formation of intracerebral Abscess
2) Development of Phlebitis –> Venous occlusion and haemorrhagic Infarction of the underlying brain
3) Scarring at the site of foramina of Luschka and Magendie –> CSF flow obstruction –> Obstructive non-communicating Hydrocephalus
4) Scarring at the arachnoidal granulations –> Reduction in CSF reabsorption –> Communicating Hydrocephalus

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cause of Aseptic Meningitis

Viral infection

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CM of Aseptic Meningitis

1) Meningeal irritation
2) Fever
3) Alterations in consciousness

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lab findings in Aseptic Meningitis

CSF:
* Lymphocytosis
* Moderate protein elevation
* Normal glucose level

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Macroscopic Features:
* Brain swelling
* subtle Hyperaemia

Microscopic Findings:
* Mild to moderate leptomeningeal lymphocytic infiltrate

features of?

Aseptic Meningitis

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cause of Tuberculous Meningitis

Mycobacterium tuberculosis

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CM of Tuberculous Meningitis

Headache
Malaise
Mental confusion
Vomiting

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lab fidings in Tuberculous Meningitis

Moderate increased cellularity; Mononuclear cells or
a mixture of polymorphonuclear and mononuclear cells
Elevated protein level
Moderately reduced or normal glucose content

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progression and complications of Tbc Meningitis

Arachnoid fibrosis –> Hydrocephalus

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Macroscopic Features:
* Gelatinous or fibrinous exudate at the base of the brain –> Obliteration of the cisterns and wrapping of cranial nerves
* Obliterative Endarteritis of the arteries in the
subarachnoid space

Microscopic Findings:
* Mixtures of lymphocytes, plasma cells and macrophages
* Well formed granulomas with caseous necrosis (florid cases)

features of?

Tbc Meningitis

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causes of Brain Abscess

Bacterial infections

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CF of Brain Abscess

Progressive focal deficits
General signs related to increased intracranial
pressure

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lab findings of Brain Abscess

Increased numbers of white blood cells
high protein levels
Normal glucose content

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Macroscopic Features: * Discrete lesion * **Central liquefactive necrosis** * Surrounding fibrous capsule Microscopic Findings: * **Granulation tissue** and **oedema** around the necrotic core * **Zone of reactive gliosis**, outside the fibrous capsule features of?

Brain Abscess

complications of Brain Abcesse 1) Increased intracranial pressure --> **-------** 2) Abscess rupture --> **------------, -----------------, and ---------**

1) Increased intracranial pressure --> **Herniation** 2) Abscess rupture --> **Ventriculitis, Meningitis, and Venous sinus Thrombosis**

Venous sinus Thrombosis --> **-------**

Haemorrhagic Venous infarction

Characteristic Histologic Features: * Perivascular and parenchymal mononuclear cell infiltrates * **Microglial nodules** * **Neuronophagia** * Presence of **inclusion bodies** features of?

Viral Encephalitis

Important cause of Epidemic Encephalitis?

**ARBO** (ARthropod-BOrne) virus

CM of ARBO (Arthropod-borne) disease

* Seizures * Confusion * Delirium * Stupor or Coma * Reflex asymmetry * Ocular Palsies * **yellow fever**

Types of ARBO (ARthropod- Borne) viruses

1) Eastern and Western Equine Encephalitis 2) West Nile virus infection

Lab findings of ARBO (Arthropod-borne) viruses

CSF: * **Colourless** * **Early neutrophilic pleocytosis** -->Conversion to lymphocytosis * Elevated protein level * Normal glucose

Microscopic Findings: * Perivascular **lymphocytic Meningoencephalitis** * **Micro-Abscess in the white matter** * Multifocal gray and white matter necrosis * **Neuronophagia** * **Microglial nodules** * Necrotising Vasculitis with focal haemorrhages (severe cases) features of?

Eastern Eqine Encephalitis (ARBO Viruses)

Epi of HSV-1 | * Herpes virus

Most common in children and young adults

CM of HSV-1

Alterations in mood, memory and behaviour

# ** Macroscopic Features: * Inferior and medial regions of the temporal lobes and the orbital gyri of the frontal lobes * **Heamorrhagic Necrosis** in the **Temporal and frontal lobe** Microscopic Findings: * Necrotising and haemorrhagic infection * Perivascular inflammatory infiltrates * Large eosinophilic intranuclear viral inclusions **(Cowdry type A bodies)** features of?

HSV Encephalitis (caused by HSV-1)

# HSV Encephalitis (caused by HSV-1) Macroscopic Features: * Inferior and medial regions of the temporal lobes and the orbital gyri of the frontal lobes * **Heamorrhagic Necrosis** in the **---------- and ---------** Microscopic Findings: * Necrotising and haemorrhagic infection * Perivascular inflammatory infiltrates * Large eosinophilic intranuclear viral inclusions **(-------------------)**

Macroscopic Features: * Inferior and medial regions of the temporal lobes and the orbital gyri of the frontal lobes * **Heamorrhagic Necrosis** in the **Temporal and frontal lobe** Microscopic Findings: * Necrotising and haemorrhagic infection * Perivascular inflammatory infiltrates * Large eosinophilic intranuclear viral inclusions **(Cowdry type A bodies)**

HSV-2 occures as: * **---------** in adults * **-------------------** in neonates, born by mothers with active primary HSV genital infections

* **Meningitis** in adults * **Disseminated severe Encephalitis** in neonates, born by mothers with active primary HSV genital infections

CM of Polio Virus

1) Muscle wasting 2) Hporefelxia 3) Death from respiratory muscles paralysis (Acute) 4) Mild Gastroenterits 5) Paralytic Poliomeylitis

Pathogensis and CM of Polio virus * Subclinical or **-------------** * Invasion of the CNS and destruction of the motor neurons in spinal cord and brain stem **(--------------)** * Loss of motor neurons --> **------------** and **--------------**, in the affected body region * Paralysis of the respiratory muscles, in acute disease --> **----------**

* Subclinical or **mild Gastroenteritis** * Invasion of the CNS and destruction of the motor neurons in spinal cord and brain stem **(Paralytic Poliomyelitis)** * Loss of motor neurons --> **Muscle wasting** and **hyporefelxia**, in the affected body region * Paralysis of the respiratory muscles, in acute disease --> **death**

# * Polio virus patho and CM of Post-Polio syndrome: * manifests **------- yrs** after the initial illness * CM: **-----------------** associated with decreased muscle bulk and pain

* manifests **25-35yrs** after the initial illness * CM: **Progressive weakness** associated with decreased muscle bulk and pain

cause of Rabis Virus

Bite from diseased animals (fox)

Pathogenesis of Rabies Virus

Ascent of the virus along the peripheral nerves from the wound site

CM of Rabies Virus

* Malaise * Headache * Fever * **Extra-ordinary CNS excitability (the slightest touch is painful)** * Contracture of the pharyngeal musculature --> **Hydrophobia** * **Periods of mania and stupor progress to coma and death**

Microscopic Findings: * Discrete, intra-cytoplasmic, deeply eosinophilic inclusions within neurons **(Negri bodies)** features of?

Rabies virus

# Rabies virus Microscopic Findings: * Discrete, intra-cytoplasmic, deeply eosinophilic inclusions within neurons **(--------------)**

**Negri bodies**

Varicella-Zoster Virus causes?

Chickenpox (primary infection)

Varicella-Zoster Virus can reactivate in adults and mainfest as?

**Shingles** (painful vesicular skin eruption in deramtomes distribution)

CM of HIV

* **Cognitive dysfunction** (ranging from mild to marked dementia) * **Aseptic [Viral] Meningitis** (1-2 weeks after onset of primary infection; 10% of patients)

Lab findings in HIV

* Antibodies to HIV * Isolation of the virus from the CSF

Microscopic Findings: * Predominantly, in **subcortical white matter, diencephalon and brain stem** * Presence of microglial nodules, with **multinucleate giant cells** * Abnormally prominent endothelial cells * Perivascular **foamy or pigment-laden macrophages** * Foci of **tissue necrosis and reactive gliosis** * Multifocal or diffuse areas of **myelin pallor**, with **axonal swellings and gliosis** * Identification of virus in **CD4+ lymphocytes** and multinucleate macrophages and microglia features of?

HIV

Myelin in the White matter can be identified using which histochemical stain ?

**LFB- Luxol Fast Blue**

cause of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

JC virus

pathogensis of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

**Infection** (preferentially) of the **oligodendrocytes** --> Oligodendrocytes’ injury and death with resultant **demyelination**

**Imaging studies of?** imaging: Extensive, often multifocal, **ring-enhancing lesions in the hemispheric or cerebellar white matter**

Polymoa-Virus & Progressive multifocal leukoencenphalopathy

CF of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

Focal and progressive neurologic symptoms and signs

Macroscopic Features: * **Patchy**, irregular, **ill-defined areas of white matter destruction** Microscopic Findings: * Centrally localised lipid-laden macrophages and reduced number of axons * In the periphery of the lesion, **enlarged oligodendrocyte nuclei (Plum-coloured)** with **glassy-appearing amphophilic viral inclusions** * **Bizarre** giant forms of **astrocytes** (irregular, hyperchromatic, sometimes multiple nuclei) features of?

Polymoa-Virus & Progressive multifocal leukoencenphalopathy

CF of Fungal Encephalitis caused by **Cryptococcus Neoformans**

* **Fulminant and fatal (2 weeks)** * **Indolent** behaviour, with development over months or years

CSF examination of Fungal Encephalitis caused by Cryptococcus neoformans show?

1) Elevated protein; 2) Mucoid encapsulated yeasts (India ink); 3) Positive test for cryptococcal Ag

Morphology: Proliferation of the organisms in the Virchow-Robin spaces --> Characteristic **“soap bubble”** like appearance Features of?

Fungal Encepahlitis caused by **Cyrptococcus Neofromans**

# Fungal encephalitis caused by cryptococcus neoformans Morphology: Proliferation of the organisms in the Virchow-Robin spaces --> Characteristic **"--------------”** like appearance

**"soap bubble"**

cause of Cerebral Toxoplasmosis

Toxoplasma gondii

Epi of Cerebral Toxoplasmosis

* Immunosuppressed adults * Newborns; trans-placentally from an infected mother

CM of Cerberal Toxoplasmosis in Adults

Subacute symptomatology, evolving within 1-2 weeks

CM of Cerebral Toxoplasmosis in Newbrons

Triad of: * Chorioretinitis (causes blurred vision) * Hydrocephalus * Intracranial calcifications

Macroscopic Features: * **Multiple Abscesses in the gray-white junction** and the deep gray nuclei (immunosuppressed individuals) * **Oedema** Microscopic Findings: * Central foci of necrosis with small haemorrhages and mixed inflammatory cell infiltrates and vascular proliferation * Free **Tachyzoites and encysted Bradyzoites** at the periphery of the necrotic foci features of?

Cerebral Toxoplasmosis

cause of Cysticercosis

Taenia solium

CM of cysticercosis

Mass lesion --> Seizures

Macroscopic Features: * **Cysts with a smooth lining**, within the brain and subarachnoid space Microscopic Findings: * **Body wall** and **hooklets** from mouth parts * **Intense inflammatory infiltrate** (with eosinophils) - incase of dead encysted organism * Marked gliosis features of?

Cysticercosis

cause of Prion disease : Abnormal form of a cellular protein; Conformational change from its normal shape **(α-Helical** **------**) to an abnormal conformation **(β-sheet** **-------**)

Abnormal form of a cellular protein; Conformational change from its **normal shape (α-Helical PrPc)** to an **abnormal conformation (β-sheet PrPsc)**

# Prion disease patho: Spontaneous change of PrPc to PrPsc conformation--> **-----------**

Sporadic form of CJD (Creutzfeldt-Jakob disease)

# Prion disease patho: Mutations in the PRNP gene (encoding PrPc) --> **---------**

**Familial form of CJD** (Creutzfeldt-Jakob disease)

Most common form of Creutzfeldt-Jakob disease

Sporadic form --> 85% of cases

Epi of Sporadic Creutzfeldt-Jakob disease

>70 years

Epi of Familial Creutzfelt-Jakob disease

Younger people

Macroscopic Features: * Little or no brain atrophy Microscopic Findings: * **Spongiform changes** in the cerebral cortex and deep gray matter structures (e.g. Nucleus caudatus, Putamen) * **Neurons w/ Microscopic vacuoles** of variable size within the neuropil and neuronal perikaryon * Severe cases: * Severe neuronal loss * Reactive (astro)gliosis * Development of **“status spongiosus”** features of?

Sporadic and Familial Creutzfeldt-Jakob disease

Vareint Cretzfeldet-Jakob disease specific microscopic diffrence from other CJD forms

**Amyloid plaques**