Neuroanatomy Flashcards

1
Q

What is a stroke and two main causes?

A

Stroke = interruption of blood supply to parts of the brain. 2 main causes:

Ischaemic- blood supply is blocked due to a blood clot (85% of all cases)

Haemorrhagic- where a weakened blood vessel supplying the brain bursts

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2
Q

diff locations of strokes and effects?

A

Anterior cerebral- loss of blood from anterior cerebral arteries will affect primary motor cortex for lower limb and perineum of contralateral side. Can lead to incontinence due to lack of control of pelvic floor muscles

Middle cerebral- blockage of blood supply here will lead to loss of sensation and motor function of body except for lower limb and perineum. Middle supply also supplies broca’s motor speech area and wernickes sensory speech area. Loss of function can affect how someone speaks and the ability to understand speech

Posterior cerebral- posterior arteries supply primary visual cortex. Blockage here can lead to visual field defects. Posterior supplies hippocampus. Blockage here can lead to memory loss

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3
Q

what is a Intracranial haemorrhage- and the 3 diff types?

A

Intracranial haemorrhage- result from trauma, cerebral lesions, or haematoma which is the enlargement of a vessel that ruptures. Different types:

Extradural haemorrhage- occurs between skull and dura mater proper. If trauma to the side of the head occurs, haemorrhage will occur in middle meningeal artery, putting pressure on local structures and raises intracranial pressure leading to herniation of cerebellum/damage to brainstem

Subdural haemorrhage- build-up of blood in subdural space (between dura and arachnoid mater). Trauma to the head can cause displacement of the skull which Leads to tearing of veins as they enter superior sagittal sinus (dural venous sinus). This causes a slow build-up of intracranial pressure, hence can appear asymptomatic at the beginning.

Subarachnoid haemorrhage- aneurysms leakage or rupture of circle of willis. Can lead to severe headache and loss of consciousness. Diagnosed by withdrawing heavily blood-stained cerebrospinal fluid through lumbar puncture

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4
Q

Bacterial meningitis-

A

acute inflammation of the arachnoid and pia with thick, creamy exudate (pus) filling the subarachnoid space

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5
Q

Hydrocephalus-

A

overproduction of CSF or blockage of ventricular system leads to accumulation of CSF. In neonatal skull increase in pressure will force unfused cranial bones to pull apart leading to cranial abnormalities. In a fused adult skull can lead to rise in intracranial pressure. Treated with shunt draining CSF from ventricular system into a body cavity where it can be reabsorbed

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6
Q

Summary of cerebral artery occlusion

A

Middle cerebral = paralysis and loss of sensation in trunk and upper limb/ loss of production and interpretation of speech

Anterior cerebral = paralysis and loss of sensation to lower limb and perineum

Posterior cerebral = visual field defects and memory loss

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7
Q

Dyskinesias-

A

excessive dopamine leads to unwanted involuntary movements

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8
Q

Parkinsons disease , symptoms and causes?

A

Parkinson’s disease- degeneration and death of neurons. Disorder of basal ganglia

Symptoms- bradykinesia, resting tremor, postural impairment/instability, lead-pipe rigidity, constipation, cognitive impairment, and psychiatric symptoms

Causes- degeneration of dopaminergic neurons of SN = low dopamine level = overactivity of indirect pathway = difficult to initiate movement.

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9
Q

Huntingtons disease , symptoms and causes?

A

Huntington’s disease- basal ganglia disorder. Inherited, progressive neurodegenerative disorder.

Symptoms- hyperkinetic and unwanted abnormal movements, impairment in co-ordination and balance, cognitive and psychiatric symptoms like psychosis and depression

Causes- Degeneration of caudate nucleus of putamen

Increase direct pathway, decrease indirect pathway = inhibition of unwanted movements

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10
Q

Anxiety/PTSD/Bipolar/panic disorder/depression-

A

amygdala disorder

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11
Q

Alzheimer disease-

A

severe atrophy of hippocampal formation leading to amnesia for recent events and inability to learn new info of an autobiographical kind i.e. loss of episodic memory

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12
Q

Semantic dementia-

A

atrophy of middle and inferior temporal neocortical gyri. Patients lose meaning of words and percept’s i.e. their knowledge of the world (semantic memory). Other symptoms include associate agnosia (don’t remember names/recognise people), episodic memory is preserved

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13
Q

Parkingsons vs huntingtons

A

Parkinsons disease - bradykinesia:
death of dopaminergic neurons of SNpc = low dopamine = decreased direct pathway and increased indirect pathway = slow movement and tremor.
other symptoms - postural impairment, lead-pipe rigidity, constipation, psychiatric and neurological symtpoms

Hungtingtons disease - excessive unwanted movements:
Degeneration of neostriatum = increased direct pathway and decreased indirect pathway = increased unwanted movement
other symptoms - hyperkinesia, dyskinesia, balance impairment, psychosis, depression. also is inherited.

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14
Q

Frontotemporal dementia (FTD)-

A

atrophy of prefrontal neocortex and amygdala, symptoms include cognitive deficits (planning/organisation/personality change), loss of primary and social emotions

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15
Q

Clinical testing for somatic sensory pathways?

A

Dorsal column pathway- fine touch, proprioception (i.e., knowing where limbs are without looking), vibration sense
-Tested using tuning fork on toe (last clin skills)

Spinothalamic tract- pain, temp, crude touch, general touch, pressure

  • Transmitted via myelinated A-delta fibres and unmyelinated C-fibres
  • Pin prick test (last clin skills)
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16
Q

Tuberculoma-

A

benign mass due to tuberculosis infection affecting anterolateral column of the spinal cord

17
Q

Clinical importance of pyramidal tract?

A

Controls voluntary movement

18
Q

Lower motor lesions =

A

paralysis or paresis (weakening) of specific muscles, loss of tendon reflex activity and reduced muscle tone. Spontaneous muscle contractions occur and effected muscles atrophy over time.
Cause: nerve supply interrupted to muscle.
Symptoms : weakness, flaccid (floppy) paralysis of muscle, complete loss of muscle tone (hypotonia), absence of deep tendon reflexes (areflexia), muscle atrophy, spontaneous muscle twitching (fasciculations)

19
Q

Upper motor neuron lesions =

A

paralysis or paresis (weakening) of movements, increased tenson reflex activity and increased muscle tone but no muscle atrophy = result of this is spasticity and hyperreflexia, clonus (involuntary rhythmic muscle contraction), clasp-knife rigidity (rapid decrease in resistance when attempting to flex a joint), hypertonia and pyramidal posture. Causes of UMNL is stroke

Damage in brain = weakness on opposite side
Damage in spinal cord = weakness is ipsilateral

20
Q

Motor neuron disease-

A

features are mixed as both upper and lower neurons are affected

21
Q

Spasticity-

A

combination of paralysis, increased tendon reflex activity and hypertonia

22
Q

Brown-sequard syndrome-

A

caused by stab wound which hemisects spinal cord

Ipsilateral loss = weakness or paralysis and proprioceptive deficits on the side of the body ipsilateral to the lesion

Contralateral loss = pain and temp sensation

23
Q

If spinothalamic tract damaged

A

If spinothalamic tract damaged and nothing else, you won’t feel pain/general touch but can still feel fine touch and proprioception

24
Q

If dorsal column pathway damaged,

A

If dorsal column pathway damaged, then you won’t feel fine touch and proprioception from the same side of damage/weakness

25
Q

Corticospinal tract damage

A

Corticospinal tract- if damage in brain/brainstem above the level of decussation then weakness on the opposite side. If damage in spinal cord and below level of decussation (medulla) then there will be muscle weakness/paralysis on the same side

26
Q

If you cut the spinal cord

A

If you cut the spinal cord, you will lose all motor and sensory innervation below the cut point

27
Q

If there has been a cut or lesion on the left side, t

A

If there has been a cut or lesion on the left side, then corticospinal tract and dorsal column tract on the same side will be affected and you will lose motor innervation and won’t feel fine touch/proprioception respectively. Spinothalamic tract coming from right side will be affected and so lesion on left side will cause loss of pain/general touch etc on right side, but they can still pain/general touch on the left side (same side as lesion)

28
Q

Clinical relevance of vagus nerve?

A

Role in relation to heart – slowing heart down e.g beta blockers, muscarinic agonsist can be used to target vagus nerve to slow down heart rate​

Damage to nerve – rare- but can lead to difficulties; swallowing difficulty, gag reflex problems,