Diseases Of The Central Nervous System at ETHZ - ETH Zurich | Flashcards & Summaries

Lernmaterialien für Diseases of the Central Nervous System an der ETHZ - ETH Zurich

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What is the definition and epidemiology of stroke?

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Stroke = rapidly progressing condition with clinical symptoms and/or signs of focal and at times global loss of cerebral function. The symptoms last more than 24 hours to lead to death with no apparent cause other than that of vascular origin


Transiroy Ischemic attack = similar symptoms or identical to stroke (mostly less severe). dysfunctions are transient and disappear within <24h


  • Stroke 2nd largest cause of death (globally) behind cardiological diseases (2016)
  • 15-20% of stroke patients die within the first 4 weeks after stroke
  • surviving patients: 
  • 1/3 recovers well, 1/3 shows deficits, but are able to cope with daily life, 1/3 need life-long care
  • 50% of stroke patients are >65 years old, 10% <40 years old
  • -> 78 billion dollars for medication and therapy in USA -> expensive


Lösung ausblenden
TESTE DEIN WISSEN

How are strokes classified 

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TESTE DEIN WISSEN

is a vascular disease affecting the CNS

  • Ischemic Stroke (80%)
    • occlusion of vessel -> reduction of blood flow -> infarction
    • throbotic
      • caused by thrombus (=blood clot built in vessels supplying the brain)
      • frequentlycorrelatedwith atherosclerosis (high cholesterol and increasing age)
      • often preceded by TIA
    • embolic
      • caused by embolus (= loose blood clot), which travels from periphery (mostly from heart)
      • often results from heart failures (dysrhythmia) or after heart surgery
  • hemorrhagic stroke (20%)
    • rupture of vessel -> bleeding into parenchyma of brain
    • leads to pressure and swelling of tissue against the skull -> mechanical damage of neurons
    • results from hypertension, aneurysms, malformation of vessels, traumatic (mechanical) injury
    • intracerebral (15%)
      • rupture of blood vessel in the brain parenchyma 
      • caused mostly by hypertension
    • subarachnoid (5%)
      • bleeding of vessel between skull and brain (often painful)
      • caused mostly aneurysm or vessel malformation
Lösung ausblenden
TESTE DEIN WISSEN

How is stroke diagnosed and how is it primary cared for?

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TESTE DEIN WISSEN

early signs: FAST

  • Face: does 1 side of the face drop (ask person to smile)
  • Arms: is 1 arm weak or numb (ask person to raise both arms, does one go down)
  • speech: is speech slurred (ask person to repeat a simple sentence, is it correct)
  • time: if person shows any of these symptoms -> ambulance or hospital imediately


Physical/ neurological examination: 

-> scoring of different function

  • swallow test: important for medication application
  • baseline ECG: indicator for embolic stroke
  • blood analysis: hyperglycaemia, electrolytes, creatine -> previous liver damage
  • assessment of risk factors: smoking, obesity, drugs (cocaine)


Diagnosis: 

  • CT: computed axial tomography
    • received in first 20 minutes at arrival to clinic
    • based on x-rays
    • fast, good available, less spatial resolution, less sensitive for acute stroke, but able to detect intracerebral hemorrahge
  • MRI: magnetic resonance imaging
    • based on magnetic fields
    • expensive, less abundant, good spatial resolution, more sensitive for acute stroke
  • cerebral angiography
    • injection contrast dye: visualize vessels -> mostly incombination with CT
    • specific investigation of occluded vessels and visualisation of structural changes 
    • also possible by MRI with contrast dye
    • middle cerebral artery occlusion -> most frequent form of stroke in humans
    • important for endovascular therapy: enter blood vessel with catheter to pull clot out
Lösung ausblenden
TESTE DEIN WISSEN

What are some primary mechanism of stroke?

Lösung anzeigen
TESTE DEIN WISSEN

Pathomechanism: insufficient blood supply, thus, lack of oxygen and nutrients

  • Ischemia: inadeguato blood supply of an organ due to mechanical obstruction
  • haemorrhage: blood leaking from circulatory system

Time is brain (130x 10^9): 

  • 32'000 neurons lost/s
  • 230 mio synapses lost/s
  • 200mio myelinated fibers lost/s
  • 8.7 hours older/ s
  • -> increases more with time
Lösung ausblenden
TESTE DEIN WISSEN

What are some secondary mechanisms of stroke?

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TESTE DEIN WISSEN

Bioenergetic failure: 

  • = brain isn't able to produce enough energy to maintain total functionality
  • approx 70% energy is needed to restore ionic gradient across membrane (-70mV: Na+, Ka+ and Ca2+pump)

Hypoxia: 

  • reduced or absent ATP-synthesis of neutrons 
  • membrane depolarization by passive influx (diffusion) Na+, intracellular excess of Ca2+ 
  • depolarisation: increase [Na+][Ca2+][Cl-][K+] 

Excitotoxicity

  • = too much excitation of CNS
  • high levels of intracellular Na+ leads to a disturbed glutamate gradient 
    • normal:high Glucose intracellular, low Glucose extracellular
    • Ischemia: Na+-dependent GLu-Transporter lead to destruction of gradient -> further membrane depolarization (via NMDA, AMPA) and increase Ca2+ influx into neurons
    • -> Ca2+ influx leads to further neurotransmitterelease
    • -> block of Glu binding sited on NMDA and AMPA is neuroprotectivein animal models
  • high levels of intracellular Ca2+ lead to: 
    • facilitated neurotransmitter release (excitatory)
    • activation of Ca2+ dependent proteases, lipase and DNAses
    • -> protein degradation, membrane lysis (cytotoxic edema), cell death
    • Production of free radical and reactive oxygen species (ROS)
Lösung ausblenden
TESTE DEIN WISSEN

What are some early treatment strategies of stroke?

Lösung anzeigen
TESTE DEIN WISSEN

every 30 minutes delay in repercussion is a 10% restive reduction in the probability of god clinical outcome


Reperfusion: restoration of normal blood supply

  • Thrombolysis: tissue plasminogen activator: t-PA (or IV alteplase)
    • cathalisator: plasminogen -> plasmin -> degrades fibrin -> deformation of blood clot 
    • t-PA is the only approved treatment for acute ischemic stroke
    • has to be applied within 4.5h after stroke onset
    • <10% of patients qualify for this treatment due to the narrow time window -> obligates imaging with CT or MRI
  • Preventive therapies: 
    • do not resolve thrombus or embolus, but prevent formation of new clot 
      • aspirin: anti-platelet
      • Heparin: anti-coagulant
  • endovascular treatment
    • removing the blood clot by guiding a catheter to the site of the blocked blood vessel in the brain (thrombectomy)
    • but also intra-arterial thrombolysis, recanalization by stunting -> endovascular therapy not superior to treatment with intravenous t-PA
  • surgical treatment (haemorrhage)
    • removal of aneurysm or closure of rupture vessels

neuroprotection: protect ischemic tissue (penumbra)

  • failed to improve outcome after stroke over last decades
  • -> showed good results in pre-clinical studies
  • -> not 1 approved treatment
Lösung ausblenden
TESTE DEIN WISSEN

What are the neural mechanism of spontaneous recovery after stroke?

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TESTE DEIN WISSEN

usually, some degree of spontaneous functional recovery (often incomplete)


three epochs of functional recovery: 

  • acute: initial hours after -> blood flow, deem, metabolism, etc
  • subacute: first days-weeks after -> time go highest repair and recovery (sensorimotor)
  • chronic: weeks-moths after -> plateau of functional recovery


patients with mild deficits show faster recovery of functions

most dramatic improvements occur within the first 30 days after stroke

in patients with more severe deficits, recovery processes can last up to 90 days


Molecular and cellular level: 

changes after stroke 

  • increased inflammation markers
  • growth associated proteins
  • cell-cycle proteins
  • growth factors
  • GABA receptor down-regulation
    • increased N-methyl-D-asp receptor binding 
    • angiogenesis
  • hyper excitability with facilitation of long-term potentiation
    • increased synaptogenesis
    • dendrite branching/spine density/ neuronal sprouting
    • cortical thickness

-> despite limited ability of CNS for plasticity and regeneration -> form of regrow and new synapses 


Neural network level:

  • restoration of function in ischemic brain area
    • reduced neural activity locally or close to infarct area
    • best recovery: return of neural activity in and around injured brain tissue
    • ischemic cor Zoe and penumbra: key roles for repair/ functional recovery
  • compensation of function by secondary brain areas
    • enhance activity in CNS areas distant from, but connected to core one
      • compensatory activation of CNS areas associated with lesioned brain areas
      • also observed during ageing and neurodegenerative diseases
    • reduced laterality of neural ageing and neurodegenerative diseases
      • excitation of corticospinal tract + training: boost/promote functionalrecovery
      • recrossing fibers more abundant from contralesional cortex can innervate the denervated spinal cord -> functionally compensate lesioned hemisphere
    • reorganisation of somatotopic maps after stroke
      • areas closed tracer C4 -> movement of limbs -> defined areas
      • acute: no change, except lesion
      • chronic: Ca neurons take one function of other areas -> adjacent somatosensory area takes over function of lesion area (map shift) 

-> more neurons -> better outcome

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TESTE DEIN WISSEN

What are neurodegenerative diseases?

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  • Pathomechaism are similar among neurodegenerative diseases 
  • different symptoms and deficits (dementia, motor deficit, etc)
  • age is major risk factor for neurodegenerative diseases 
  • etiology still poorly understood -> mostly symptomatic treatment 
  • are progressive diseases
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TESTE DEIN WISSEN

What is the epidemiology and of Parkinson's disease 

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  • second most frequent neurodegenerative disorder (after Alzheimers)
  • chronic, slowly progressive 
  • prevalence increases with age
  • only approx 10% of all PD cases occur on people under 45 y.o.
  • 45% without genetic etiology -> cause unknown
  • 5% genetic origin -> says a lot about pathomechanism
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TESTE DEIN WISSEN

What are the motor symptoms of Parkinson's disease?

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TESTE DEIN WISSEN
  • Parkinsonism
    • neurological syndrome that shares symptoms of PD
    • common criteria is bradykinesia and at least one of the symptoms including tremor, postural instability and rigidity
  • early motor symptoms: 
    • asymmetrical onset of deficits -> gradual spread to contralateral. side 
    • asymmetric resting tremor (3-6Hz): decreases with voluntary movement
    • development of bradykinesia (slow movement/ reflexes, small steps, micrographic, hypophonis)
  • motor symptoms in progressed PD:
    • advanced bradykinesia: most disabling motor symptom
    • hypokinesia: decreases amplitude of movement
    • akinesia: absence of movement 
    • muscular rigidity (propulsion during walking, stiff arms without swing, cogwheel)
    • postural instability at later stages: risk of falling
  • parkinsonian gait: 
    • propulsion of upper body (=festination)
    • reduced arm swing
    • reduced walkingspeed
    • reduced step length
    • shuffling steps
    • tripping gait -> very typical feature/ main pathological feature
      • visual cues help: concentration on point -> additional sensory input
Lösung ausblenden
TESTE DEIN WISSEN

How is Parkinson's disease diagnosed?

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TESTE DEIN WISSEN

1) identification of Parkinsonism (80% cases how Parkinsonism)

2) exclusion of alternative factor causing Parkinsonism 

  • drug induce
  • metabolic dysfunction
  • post-infectus
  • post-traumatic parkinsonism
  • toxin-induced
  • in the context of other neurological diseases (Alzheimer, MS,etc)

3) identification of supportive features

  • olfactory assessment 
  • response to  levodopa (L-DOPA) -> most important treatment for early and mid stages of PD
Lösung ausblenden
TESTE DEIN WISSEN

What are some categories and their characteristics of CNS pathologies?

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TESTE DEIN WISSEN
  • Neurodegenerative disease 
    • Alzheimer's Disease
    • Prakinson's Disease
    • Amyotrophic lateral sclerosis (ALS)
    • Huntington's Disease
  • Psychiatric disorders 
    • bipolar disorders
    • Schizophrenia
    • autism
  • autoimmune diseases
    • multiple sclerosis (MS)
    • myasthenia gravis
  • neuroinfection diseases
    • meningitis (viral or bacterial)
    • encephalitis (viral or bacterial)
  • traumatic insults
    • concusion
    • spinal cord injury


characteristics

  • CNS has only limited capacity for regeneration and plasticity
  • peripheral nerve fibers are capable of regeneration
  • stabilisation of network -> persisting connection and no aberrant connection (evolutionary advantage)
  • physiological facts: 
    • consumes approx 20% of all oxygen
    • consumes approx 25% of total energy consumption (mainly glucose of body)
    • blood-brain barrier: maintenance of CNS,homoestasis and immune-privilege$no pain receptors (nociceptors) in CNS parenchyma (only in meninges)
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Q:

What is the definition and epidemiology of stroke?

A:

Stroke = rapidly progressing condition with clinical symptoms and/or signs of focal and at times global loss of cerebral function. The symptoms last more than 24 hours to lead to death with no apparent cause other than that of vascular origin


Transiroy Ischemic attack = similar symptoms or identical to stroke (mostly less severe). dysfunctions are transient and disappear within <24h


  • Stroke 2nd largest cause of death (globally) behind cardiological diseases (2016)
  • 15-20% of stroke patients die within the first 4 weeks after stroke
  • surviving patients: 
  • 1/3 recovers well, 1/3 shows deficits, but are able to cope with daily life, 1/3 need life-long care
  • 50% of stroke patients are >65 years old, 10% <40 years old
  • -> 78 billion dollars for medication and therapy in USA -> expensive


Q:

How are strokes classified 

A:

is a vascular disease affecting the CNS

  • Ischemic Stroke (80%)
    • occlusion of vessel -> reduction of blood flow -> infarction
    • throbotic
      • caused by thrombus (=blood clot built in vessels supplying the brain)
      • frequentlycorrelatedwith atherosclerosis (high cholesterol and increasing age)
      • often preceded by TIA
    • embolic
      • caused by embolus (= loose blood clot), which travels from periphery (mostly from heart)
      • often results from heart failures (dysrhythmia) or after heart surgery
  • hemorrhagic stroke (20%)
    • rupture of vessel -> bleeding into parenchyma of brain
    • leads to pressure and swelling of tissue against the skull -> mechanical damage of neurons
    • results from hypertension, aneurysms, malformation of vessels, traumatic (mechanical) injury
    • intracerebral (15%)
      • rupture of blood vessel in the brain parenchyma 
      • caused mostly by hypertension
    • subarachnoid (5%)
      • bleeding of vessel between skull and brain (often painful)
      • caused mostly aneurysm or vessel malformation
Q:

How is stroke diagnosed and how is it primary cared for?

A:

early signs: FAST

  • Face: does 1 side of the face drop (ask person to smile)
  • Arms: is 1 arm weak or numb (ask person to raise both arms, does one go down)
  • speech: is speech slurred (ask person to repeat a simple sentence, is it correct)
  • time: if person shows any of these symptoms -> ambulance or hospital imediately


Physical/ neurological examination: 

-> scoring of different function

  • swallow test: important for medication application
  • baseline ECG: indicator for embolic stroke
  • blood analysis: hyperglycaemia, electrolytes, creatine -> previous liver damage
  • assessment of risk factors: smoking, obesity, drugs (cocaine)


Diagnosis: 

  • CT: computed axial tomography
    • received in first 20 minutes at arrival to clinic
    • based on x-rays
    • fast, good available, less spatial resolution, less sensitive for acute stroke, but able to detect intracerebral hemorrahge
  • MRI: magnetic resonance imaging
    • based on magnetic fields
    • expensive, less abundant, good spatial resolution, more sensitive for acute stroke
  • cerebral angiography
    • injection contrast dye: visualize vessels -> mostly incombination with CT
    • specific investigation of occluded vessels and visualisation of structural changes 
    • also possible by MRI with contrast dye
    • middle cerebral artery occlusion -> most frequent form of stroke in humans
    • important for endovascular therapy: enter blood vessel with catheter to pull clot out
Q:

What are some primary mechanism of stroke?

A:

Pathomechanism: insufficient blood supply, thus, lack of oxygen and nutrients

  • Ischemia: inadeguato blood supply of an organ due to mechanical obstruction
  • haemorrhage: blood leaking from circulatory system

Time is brain (130x 10^9): 

  • 32'000 neurons lost/s
  • 230 mio synapses lost/s
  • 200mio myelinated fibers lost/s
  • 8.7 hours older/ s
  • -> increases more with time
Q:

What are some secondary mechanisms of stroke?

A:

Bioenergetic failure: 

  • = brain isn't able to produce enough energy to maintain total functionality
  • approx 70% energy is needed to restore ionic gradient across membrane (-70mV: Na+, Ka+ and Ca2+pump)

Hypoxia: 

  • reduced or absent ATP-synthesis of neutrons 
  • membrane depolarization by passive influx (diffusion) Na+, intracellular excess of Ca2+ 
  • depolarisation: increase [Na+][Ca2+][Cl-][K+] 

Excitotoxicity

  • = too much excitation of CNS
  • high levels of intracellular Na+ leads to a disturbed glutamate gradient 
    • normal:high Glucose intracellular, low Glucose extracellular
    • Ischemia: Na+-dependent GLu-Transporter lead to destruction of gradient -> further membrane depolarization (via NMDA, AMPA) and increase Ca2+ influx into neurons
    • -> Ca2+ influx leads to further neurotransmitterelease
    • -> block of Glu binding sited on NMDA and AMPA is neuroprotectivein animal models
  • high levels of intracellular Ca2+ lead to: 
    • facilitated neurotransmitter release (excitatory)
    • activation of Ca2+ dependent proteases, lipase and DNAses
    • -> protein degradation, membrane lysis (cytotoxic edema), cell death
    • Production of free radical and reactive oxygen species (ROS)
Mehr Karteikarten anzeigen
Q:

What are some early treatment strategies of stroke?

A:

every 30 minutes delay in repercussion is a 10% restive reduction in the probability of god clinical outcome


Reperfusion: restoration of normal blood supply

  • Thrombolysis: tissue plasminogen activator: t-PA (or IV alteplase)
    • cathalisator: plasminogen -> plasmin -> degrades fibrin -> deformation of blood clot 
    • t-PA is the only approved treatment for acute ischemic stroke
    • has to be applied within 4.5h after stroke onset
    • <10% of patients qualify for this treatment due to the narrow time window -> obligates imaging with CT or MRI
  • Preventive therapies: 
    • do not resolve thrombus or embolus, but prevent formation of new clot 
      • aspirin: anti-platelet
      • Heparin: anti-coagulant
  • endovascular treatment
    • removing the blood clot by guiding a catheter to the site of the blocked blood vessel in the brain (thrombectomy)
    • but also intra-arterial thrombolysis, recanalization by stunting -> endovascular therapy not superior to treatment with intravenous t-PA
  • surgical treatment (haemorrhage)
    • removal of aneurysm or closure of rupture vessels

neuroprotection: protect ischemic tissue (penumbra)

  • failed to improve outcome after stroke over last decades
  • -> showed good results in pre-clinical studies
  • -> not 1 approved treatment
Q:

What are the neural mechanism of spontaneous recovery after stroke?

A:

usually, some degree of spontaneous functional recovery (often incomplete)


three epochs of functional recovery: 

  • acute: initial hours after -> blood flow, deem, metabolism, etc
  • subacute: first days-weeks after -> time go highest repair and recovery (sensorimotor)
  • chronic: weeks-moths after -> plateau of functional recovery


patients with mild deficits show faster recovery of functions

most dramatic improvements occur within the first 30 days after stroke

in patients with more severe deficits, recovery processes can last up to 90 days


Molecular and cellular level: 

changes after stroke 

  • increased inflammation markers
  • growth associated proteins
  • cell-cycle proteins
  • growth factors
  • GABA receptor down-regulation
    • increased N-methyl-D-asp receptor binding 
    • angiogenesis
  • hyper excitability with facilitation of long-term potentiation
    • increased synaptogenesis
    • dendrite branching/spine density/ neuronal sprouting
    • cortical thickness

-> despite limited ability of CNS for plasticity and regeneration -> form of regrow and new synapses 


Neural network level:

  • restoration of function in ischemic brain area
    • reduced neural activity locally or close to infarct area
    • best recovery: return of neural activity in and around injured brain tissue
    • ischemic cor Zoe and penumbra: key roles for repair/ functional recovery
  • compensation of function by secondary brain areas
    • enhance activity in CNS areas distant from, but connected to core one
      • compensatory activation of CNS areas associated with lesioned brain areas
      • also observed during ageing and neurodegenerative diseases
    • reduced laterality of neural ageing and neurodegenerative diseases
      • excitation of corticospinal tract + training: boost/promote functionalrecovery
      • recrossing fibers more abundant from contralesional cortex can innervate the denervated spinal cord -> functionally compensate lesioned hemisphere
    • reorganisation of somatotopic maps after stroke
      • areas closed tracer C4 -> movement of limbs -> defined areas
      • acute: no change, except lesion
      • chronic: Ca neurons take one function of other areas -> adjacent somatosensory area takes over function of lesion area (map shift) 

-> more neurons -> better outcome

Q:

What are neurodegenerative diseases?

A:
  • Pathomechaism are similar among neurodegenerative diseases 
  • different symptoms and deficits (dementia, motor deficit, etc)
  • age is major risk factor for neurodegenerative diseases 
  • etiology still poorly understood -> mostly symptomatic treatment 
  • are progressive diseases
Q:

What is the epidemiology and of Parkinson's disease 

A:
  • second most frequent neurodegenerative disorder (after Alzheimers)
  • chronic, slowly progressive 
  • prevalence increases with age
  • only approx 10% of all PD cases occur on people under 45 y.o.
  • 45% without genetic etiology -> cause unknown
  • 5% genetic origin -> says a lot about pathomechanism
Q:

What are the motor symptoms of Parkinson's disease?

A:
  • Parkinsonism
    • neurological syndrome that shares symptoms of PD
    • common criteria is bradykinesia and at least one of the symptoms including tremor, postural instability and rigidity
  • early motor symptoms: 
    • asymmetrical onset of deficits -> gradual spread to contralateral. side 
    • asymmetric resting tremor (3-6Hz): decreases with voluntary movement
    • development of bradykinesia (slow movement/ reflexes, small steps, micrographic, hypophonis)
  • motor symptoms in progressed PD:
    • advanced bradykinesia: most disabling motor symptom
    • hypokinesia: decreases amplitude of movement
    • akinesia: absence of movement 
    • muscular rigidity (propulsion during walking, stiff arms without swing, cogwheel)
    • postural instability at later stages: risk of falling
  • parkinsonian gait: 
    • propulsion of upper body (=festination)
    • reduced arm swing
    • reduced walkingspeed
    • reduced step length
    • shuffling steps
    • tripping gait -> very typical feature/ main pathological feature
      • visual cues help: concentration on point -> additional sensory input
Q:

How is Parkinson's disease diagnosed?

A:

1) identification of Parkinsonism (80% cases how Parkinsonism)

2) exclusion of alternative factor causing Parkinsonism 

  • drug induce
  • metabolic dysfunction
  • post-infectus
  • post-traumatic parkinsonism
  • toxin-induced
  • in the context of other neurological diseases (Alzheimer, MS,etc)

3) identification of supportive features

  • olfactory assessment 
  • response to  levodopa (L-DOPA) -> most important treatment for early and mid stages of PD
Q:

What are some categories and their characteristics of CNS pathologies?

A:
  • Neurodegenerative disease 
    • Alzheimer's Disease
    • Prakinson's Disease
    • Amyotrophic lateral sclerosis (ALS)
    • Huntington's Disease
  • Psychiatric disorders 
    • bipolar disorders
    • Schizophrenia
    • autism
  • autoimmune diseases
    • multiple sclerosis (MS)
    • myasthenia gravis
  • neuroinfection diseases
    • meningitis (viral or bacterial)
    • encephalitis (viral or bacterial)
  • traumatic insults
    • concusion
    • spinal cord injury


characteristics

  • CNS has only limited capacity for regeneration and plasticity
  • peripheral nerve fibers are capable of regeneration
  • stabilisation of network -> persisting connection and no aberrant connection (evolutionary advantage)
  • physiological facts: 
    • consumes approx 20% of all oxygen
    • consumes approx 25% of total energy consumption (mainly glucose of body)
    • blood-brain barrier: maintenance of CNS,homoestasis and immune-privilege$no pain receptors (nociceptors) in CNS parenchyma (only in meninges)
Diseases of the Central Nervous System

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