Neurology- Hx and some examination Flashcards

1
Q

Anatomy and physiology
Re: cell biology

A
  • The nervous system consists of the brain and spinal cord (CNS) and the peripheral nervous system (PNS)
    -PNS is responsible for controlling involuntary movements
  • Each neuron has a cell body and axon terminating at the synapse, supported by astrocyte and microglial cells
    -Astrocytes provide the structural framework for neurons, control their biochemical environment and form the BBB.
    -Microglial cells provide immune and scavenging functions
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2
Q

What is the anatomy of the CNS

A

-The brain has 2 cerebral hemispheres, each with 4 lobes
- Frontal, Temporal, Occipital and Parietal)
-The brain stem- consists of the pons, midbrain and medulla
- The cerebellum-
-Between the brain and the skull are 3 membranes- Dura mater (next to bone), Arachnoid and pia mater (next to nerves) with the subarachnoid space between the pia mater and arachnoid layer being filled with CSF
-Spinal cord consists of afferent and efferent neurons running too and from the brain

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3
Q

The history- inc 2 key questions

A

-Hx is often key for diagnosis
-Some Sx including LOC, amnesia may require collateral Hx
KEY QUESTIONS
1)Where (in the nervous system) is the lesion
2) What is the lesion
-Neurological Sx may be difficult to describe “blackout, dizzy, weakness” etc. Need to clarify meaning with patients

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4
Q

Time relationships and precipitating factors (good questions to ask)

A

Time
- Onset, duration and pattern of Sx over time often provide good clues e.g.
-When did the Sx start (or when was the patient last well?)
-Are they persistent or intermittent?
-If persistent are they getting better vs worse vs staying the same?
- Was the onset gradual or sudden?
Precipitating factors
-What was the pt doing when the Sx occurred?
-Does anything make it better or worse? (time of day, posture, meds)

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5
Q

Common presenting Sx- Primary Headache

A
  • The most common neurological Sx and can either be primary or secondary to other pathology.
    -Primary causes
  • Migraine
    -Tension-type
    -Trigeminal autonomic cephalalgias (include cluster)
    -Exertional headache
    -Primary thunderclap headache
    -New daily persistent type headache
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6
Q

Common presenting Sx-Secondary Headache

A
  • Includes potentially life-threatening or disabling causes
    -Such as SAH or temporal arteritis
    -One key Hx aspects is rapidity of onset
    • Isolated headache with a truly rapid onset may represent a potentially serious cause
      -Where as recurrent headache is much more likely to be migraine, particularly if patients have associated Sx
      -Asking patients what they do when they have a headache can be instructive
  • E.g. abandoning normal tasks and seeking a dark/quiet room vs pacing and agitation or even head banging in cluster headaches
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7
Q

Common presenting Sx- Transient Loss of Consciousness (TLOC)

A
  • Syncope is a LOC due to inadequate cerebral perfusion and is the most common cause of TLOC
  • Vasovagal (reflex) syncope is the most common type and is precipitated by the stimulation of the parasympathetic nervous system by factors such as pain or intercurrent illness
    -Exercise-induced syncope or syncope with no warning trigger suggests possibly cardiac in origin
    -TLOC on standing suggests postural hypotension and may be caused by drugs or autonomic neuropathies
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8
Q

Common presenting Sx- Seizure

A
  • An epileptic seizure is caused by paroxysmal electrical discharge from either the whole brain (generalised seizure) or part of the brain (focal seizure)
    -A tonic clonic seizure (convulsion) is the most common type of generalised seizure
    • Early LOC => Body stiffness (tonic phase) => Rhythmical jerking for 30- (clonic phase) => unresponsive period and finally confusion/amnesia (postictal phase)
  • A focal seizure may not involve loss of awareness and is characterised by whichever part of the brain is affected
  • You can get pseudoseizures which can be difficult to distinguish but often occur multiple times a day.
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9
Q

Common presenting Sx- Focal neurological Sx due to stroke or TIA

A
  • In a TIA Sx resolve within 24hrs
  • TIA’s are important risk factors for having future strokes and demand urgent Ax/Tx
  • Isolated vertigo, amnesia and TLOC are rare if ever in stroke
    -Haemorrhagic stroke- Hx or exam that will increase the likliehood of haemorrhagic is anti-coag use, headache, vomiting, siezures and reduced GCS
    -Spinal strokes are rare and can lead to sudden paralysis
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10
Q

Common presenting Sx- Dizziness and vertigo

A
  • Patients use dizziness to describe many sensations with recurrent dizzy spells affecting 30% of people >65 due to postural drops, CVD, arrhythmia
    -Vertigo (the illusion of movement) specifically indicates a problem within the vestibular apparatus (peripheral or less likely central)
  • As a general guide- episodes of veritgo lasting a few seconds are likely BPPV, vertigo lasting hours may be caused by Meniere’s disease (other Sx inc: hearing loss, tinnitus, N&V) or Migrainous vertigo (with or without headache)
    -Brain stem or cerebellar stroke may also present with vertigo, often associated with ataxia, diplopia and other motor/sensory Sx
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11
Q

PMH

A
  • Symptoms that the pt has forgotten about or overlooked may be important
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12
Q

Dhx

A
  • Drugs can give rise to neurological Sx
    -E.g. phenytoin can cause ataxia, excessive analgesia = overuse headache
    -Recent vaccinations may be relevant when faced with rapidly progressive weakness (Guillain-Barre Syndrome) or cerebral venous thrombosis (COVID)
    -The absence of vaccines could also provide a clue (measles, polio)
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13
Q

FHx

A
  • Some neurological conditions are genetic
    -Single-gene defects e.g Huntington’s, myotonic dystrophy
    -Others are polygenic
    -Some diseases such as PD or MND may be single-gene disorders or sporadic
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14
Q

Shx

A
  • See how the patient is dealing with the Sx, i.e mobility, ADL, POC
  • Do they drive? may need to stop them driving
    -Alcohol use (seizure, ataxia, dementia and neuropathy)
    -Vitamin deficiency- vegans may be B12 deficient
    -Recreational drugs- NO and cocaine
  • Sexually transmitted diseases such as syphillis or HIV
    -Travel disease- Lyme (facial palsy), Neurocysticerosis (Brain lesion and epilepsy), malaria (coma)
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15
Q

The Physical Examination- Assessment of conscious level
2 main parts

A

1) The state of cansciousness depends largely on the integrity of the ascending reticular activating system, which extends from the brainstem to the thalamus
2) The content of consciousness refers to how aware the person is and depends on the cerebral cortex, the thalamus and their connections
- Use the GCS as a reliable reproducible tool

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16
Q

The Physical Examination- Meningeal irritation

A
  • Meningism (inflammation of meningies) can lead to resistance to passive flexion of the neck (stiffness) or the extended leg (Kernig’s sign)
    -Meningism suggests infection or SAH but can occur with non neurological infections e.g. UTI vs CAP
  • The absence of meningism does not exclude pathology within the subsarachnoid space. In the absence of all 3 signs (fever, stigg neck and altered mental state) virtually eliminates the diagnosis in immunocompetent patients
17
Q

Meningeal irritation- Neck stiffness and Kernig’s sign

A

Neck stiffness
- Place hands either side of the head supporting the occiput (back of head)
-Chin to chest gnetly ?pain and hold for 10s. If neck stiffness is present, the neck can not be passively flexed and you may feel spasm in the neck muscles
Kernig’s sign
-Flex 1 of the pts legs to 90 degrees at both the hip and knee. Place one hand on the hamstring
-Extend the knee whilst in flexion, look at the other leg for any reflex flexion.
-Kernig’s sign is positive when extension is resisted by spasms in the hamstring
-Kernig’s sign is absent with local causes of neck stiffness

18
Q

The Physical Examination- Speech

A

-Dysarthia refers to altered or abnormal speech caused by articulation problems due to a motor defect
-Dysphonia describes the loss of volume caused by laryngeal disorders. Both affect speech only, dysarthia may affect reading/writing
-Cerebellar dysarthia- slow and slurred speech similar to alcohol intoxication
-Myasthenia gravis- Fatiguing speech that decomes more nasally and may disapear
- PD- Dysarthia/Dysphonia, monotonus voice, words running into eachother

19
Q

Dysphasia- Anatomy

A

-The language areas are located in the dominant cerebral hemisphere, which is left in most right handed people
-Broca’s area (inferior frontal region) is concerned with word production and language expression
-Wernicke’s area (Superior posterior temporal lobe) manages comprehension of spoken language
-Expressive dysphasia (motor) occurs due to dysfunction in the Broca’s area (reduced verbal output and errors in grammar but comprehension in tact)
-Receptive (sensory) dysphagia occurs due to dysfunciton in Wernicke’s area. The poor comprehenion and although speech is fluent it is meaningless

20
Q

Cortical function

A
  • Thinking, emotions, language, behaviour, planning and initiation of movements and perception of sensory information occur in the cerebral cortex
21
Q

Frontal lobe damage may cause

A
  • Personality and behaviour changes
  • Loss of emotional responsiveness
    -Dysphasia
    -Urinary incontinence
    -Primative reflexes (e.g. grasping)
  • Focal motor seizures
22
Q

Temporal lobe damage may cause

A
  • memory impairment
  • Focal seizures with psychic symptoms
    -Receptive dysphasia
23
Q

Parietal lobs damage may cause-

A
  • Cortical sensory impairments
    -Contralateral lower quadrantanopia
  • Dyslexia, dyscalculia, dysgraphia
    -Apraxia- inability to carry out complex tasks despite having intact sensory and motor centres