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Flashcards in CM- Intro to CNS Deck (96)
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1
Q

Why sulcus divides the frontal and parietal lobes of the brain?
What gyrus is found just anterior and posterior to the sulcus?

A

The central sulcus divides frontal and parietal lobes.

Frontal lobe- primary motor cortex [causes movement of contralateral body]

Parietal lobe- primary somatosensory cortex [receives senses from contralateral body]

2
Q

In what hemisphere of the brain can the following be found:

  1. primary motor cortex
  2. primary somatosensory cortex
  3. primary auditory cortex
  4. primary visual cortex?
A
  1. frontal [just in front of central sulcus]
  2. parietal [just behind central sulcus]
  3. temporal [just below sylvian fissure]
  4. occipital

These are on both sides of the brain

3
Q

What is the location and function of Broca’s area and Wernicke’s area?

A

Broca’s is on the left inferior frontal gyrus and controls the motor function of speech.

Wernicke’s is on the left posterior superior temporal gyrus and controls speech comprehension

4
Q

What are the forebrain components of the basal ganglia?

A
  1. caudate
  2. putamen
  3. globus pallidus
5
Q

What is the purpose of the internal capsule?

A

It is white matter that contains axons from cerebral hemispheres to targets in the brainstem and spinal cord [corticospinal fibers]

The fibers form the cerebral peduncles of the midbrain [on the brainstem]

6
Q

What brain structures are responsible for the motor system [planning, initiation, cessation of movement]?

A

Forebrain:

  1. caudate
  2. putamen
  3. globus pallidus

Diencephalon:
1. subthalamic nuclei [STN]

Midbrain
1. Substantia nigra

7
Q

A person has lesions in the central white matter and corpus collosum. What is your first reaction?

A
  1. MS

2. leukodystrophies

8
Q

At autopsy, a patient has atrophied caudate and putamen. What is this a prominent feature of?

A

Huntington’s disease

9
Q

The hippocampus is located on the ____________________________ and plays a critical role in _______________________.
It is usually one of the first areas to be damaged in what 2 situations?

A

It is on the medial aspect of the temporal lobe and plays a role in the formation of memory/learning.

It is one of the first areas to be injured in Alzheimer’s and generalized ischemic injury

10
Q

What portion of the brain is supplied by the:

  1. anterior cerebral artery (ACA)
  2. middle cerebral artery {MCA}
  3. posterior cerebral artery {PCA}
A
  1. medial aspects of each hemisphere
  2. lateral aspect of each hemisphere
  3. occipital cortex, inferior parieto-temporal cortex
11
Q

What is the portion of the brain that lies between the cerebrum and the brainstem?
What 4 components make up this area?

A

Diencephalon lies between the cerebrum and the brainstem.

  1. thalamus
  2. hypothalamus
  3. epithalamus [pineal gland]
  4. subthalamus
12
Q

What are the 3 major functions of the thalamus?

What nuclei correlate with each function?

A
  1. Sensory
    - ventral posterior [somatosensory]
    - lateral geniculate [visual]
    - medial geniculate [auditory]
  2. Motor
    - ventral anterior
    - ventral lateral
  3. limbic and cognitive function
    - anterior thalamic
    - pulvinar nucleus
13
Q

What is the role of the hypothalamus?

A
  1. regulate homeostasis by:
    - temp regulation
    - food and water intake
    - endocrine function [metabolism]
    - memory
  2. send trophic hormones to the ant. pituitary to regulate hormone release
14
Q

What is the role of the pineal gland?

A

It is a source of melatonin and regulates circadian rhythm

15
Q

What is the role of the subthalamus?

What happens if it is damaged?

A

It is the diencephalon component of the basal ganglia. [STN is in the “indirect” movement pathway].

If the subthalamus is damaged, it will result in hemiballism [involuntary flinging movements of contralateral limb]

16
Q

What are the major landmarks of the midbrain of the brainstem?

A
  1. cerebral peduncles
  2. superior colliculi
  3. inferior colliculi
  4. red nucleus
  5. substantia nigra
  6. ascending sensory axons
  7. posterior commisure
  8. cranial nerve nuclei
17
Q

What axons travel through the cerebral penduncles of the midbrain?
What axons travel through the ascending sensory axons?

A

Cerebral peduncles:
1. axons to the brainstem
2. corticospinal axons to the spinal cord
[separated by interpeduncular fossa]

Ascending sensory:
1. medial leminiscus
2. anterolateral pathway
[located in the tegmentum]

18
Q

What is the purpose of the substantia nigra and raphe nuclei of the midbrain?

A

Substantia nigra- [pars compacta] is a source of dopamine

Raphe nuclei- source of serotonin

19
Q

What is the job of the following structures of the midbrain:

  1. red nucleus
  2. superior colliculus
  3. inferior colliculus
  4. posterior commissure
A
  1. relays signals btw cerebellum and thalamus; cerebellum and inferior olive
  2. rapid reflexive movement of the head and eyes to sensory stimuli
  3. auditory relay nucleus
  4. carries axons involved in consensual light reflex
20
Q

What 3 cranial nerve nuclei are located in the midbrain?

A
  1. oculomotor complex [3]
  2. Edinger-Westphal nucleus
  3. trochlear nucleus [4]
21
Q

What are the 3 major structures of the pons?

What is the role of each?

A
  1. Basal pons :
    - basal pontine nuclei cross the midline and travel to the contralateral cerebellar hemisphere
    - axons descend to the medulla and spinal cord
  2. ascending sensory axons
    - medial leminiscus
    -anterolateral pathway
    [located in pontine tegmentum]
  3. locus ceruleus
    - noradrenergic projections
    - raphe nuclei
22
Q

What are the cranial nerve nuclei of the pons?

A
  1. trigeminal nuclei [5]
  2. abducens [6]
  3. facial [7]
  4. vestibulocochlear [8]
23
Q

What are the 3 major structures of the medulla oblongata?

What is the function of each?

A
  1. Pyramids
    - descending motor axons [85% cross, 15% ipsi]
  2. Olives
    - climbing fibers cross and ascend to contralateral cerebellum
  3. Medial leminiscus
    - decussating fine touch, proprioception fibers that originated in the gracile and cuneate nuclei
    - ascending anterolateral pain/temp fibers
24
Q

What CN originate in the medulla?

A
  1. spinal trigeminal [5]
  2. hypoglossal [12]
  3. dorsal motor nucleus of the vagus [X]
  4. nucleus ambiguus
  5. solitary nucleus
  6. vestibular [8]
  7. cochlear
25
Q

What 4 vessels supply the rostral brainstem?

A
  1. posterior cerebral artery [PCA]
  2. superior cerebellar artery
  3. anterior inferior cerebellar artery
  4. basilar artery
26
Q

What 4 vessels supply the caudal brainstem?

A
  1. vertebral arteries
  2. anterior spinal
  3. posterior spinal
  4. posterior inferior cerebellar artery
27
Q

What is the function of the following nerves:

  1. oculomotor
  2. trochlear
  3. trigeminal
  4. abducens
  5. facial
A
  1. MR, SR, IR, IO, levator palpebrae superioris, parasympathetic motor axons from EW to ciliary ganglion of the eye
  2. SO
  3. muscles of mastication, tensor tympani ; sensory from face; mechanoreceptor from oral cavity
  4. LR
  5. facial expression, stapedius, parasympathetic to lacrimal, submandibular, sublingual; taste from ant 2/3; pain from ear
28
Q

What is the function of the following nerves:

  1. vestibulocochlear
  2. glossopharyngeal
  3. vagus
  4. spinal accessory
  5. hypoglossal
A
  1. inner ear sensory
  2. stylopharyngeus [swallowing], parasym to parotid; taste from post 1/3; baro/chemoreceptors; pain from ear
  3. larynx, pharynx; parasymp to thoracic/abdominal viscera; epiglottis; pain from ear
  4. pharyngeal, laryngeal, SCM, trapezius muscles
  5. muscles of tongue
29
Q

What are the 3 functional divisions of the cerebellum and what is the role of each?

A
  1. vestibulocerebellum - flocculi and nodulus control balance and eye movements
  2. spinocerebellum - vermis [except nodulus and paravermal cortex] controls axial and distal muscles
  3. neocerebellum - motor memory and execution of complex motions
30
Q

If there is damage to the hemisphere of the cerebellum, where would you notice the damage?
What would the problem be?

A

Hemispheric damage to the cerebellum results in IPSILATERAL abnormalities in fine motor control.

31
Q

Describe the presentation of a midline/vermal lesion of the cerebellum. What side of the body is affected? What is the problem?

A

Vermal lesions result in :

  • abnormal balance
  • abnormal gait [ataxia]
  • abnormal eye movements

on BOTH sides of the body

32
Q

What is blood supply to the cerebellum?

A
  1. paired PICAs [post, inf. cerebellar arteries]
  2. AICAs [ant. inf, cerebellar arteries
  3. superior cerebellar arteries
33
Q

In the spinal cord, where do motor neurons lie?

What 2 diseases affect these neurons specifically?

A

Motor neurons lie in the ventral grey matter and are the target of:

  1. ALS
  2. spinal muscular atrophy
34
Q

What are the descending motor tracts of the spinal cord and where are they located?

A

85% of the descending motor neurons cross in the pyramids of the medulla and run in the contralateral lateral corticospinal tracts.

[lateral white matter]

35
Q

What nuclei are in the dorsal columns of the spinal cord?

What do the axons convey information about? From what part of the body?

A

The dorsal columns contain the gracile and cuneate fasiculi.

Cuneate - C1 to T6 so fine touch, proprioception, vibration from the arms/upper body
Gracile - fine touch, proprioception, and vibration from the lower extremities

36
Q

What is blood supply to the spinal cord?

A
  1. anterior spinal artery [front 2/3]
  2. posterior spinal arteries [posterior 1/3]
  3. radicular arteries
37
Q

Describe the pathway of the descending corticospinal tracts.

A
  1. Primary motor cortex [just in front of central sulcus]
  2. posterior limb of internal capsule to ipsilateral cerebral peduncles of midbrain
  3. In the pyramids of the medulla 85% of fibers cross and continue in the contralateral corticospinal tract, while 15% remain ipsilateral
  4. synapse on neurons of the anterior horn
38
Q

Injury to motor neurons or their descending axons cause what type of symptoms?

A

UMN signs and symptoms like:

  1. weakness
  2. spasticity
  3. hyper-reflexia
39
Q

If an injury to the corticospinal pathway occurs rostral to the decussation in the medullary pyramids, the UMN signs will be on the _____________ side of the body as the lesion.
If the injury occurs below the level of the medulla, the UMN manifestations will be on the ____________ side as the lesion.

A

Above the medulla- motor symptoms will be on the contralateral side of the lesion

Below the medulla- motor symptoms will be on the same side of the lesion

40
Q

What are the 2 ascending sensory pathways?

A
  1. dorsal column- medial leminiscus system [proprioception, fine touch, vibration]
  2. anterolateral [pain, temperature]
41
Q

Describe the dorsal column-medial leminiscus pathway.

A
  1. dorsal root ganglia ascend ipsilaterally through gracile and cuneate fasiculi
  2. Axons synapse on cuneate and gracile nuclei in the medulla
  3. medial leminiscus crosses the midline and ascends rostrally to the ventral posterior lateral [VPL] nucleus of the thalamus
  4. VPL synapse on primary somatosensory cortex
42
Q

Describe the spinothalamic/anterolateral pathway.

A
  1. sensory axons synapse on dorsal horn of spinal column [Lissaur’s tracts]
  2. cross midline immediately and ascend to VPL
  3. Pain and temp fibers from VPL go to primary somatosensory cortex
43
Q

What symptoms are noted with a lateral hemisection of the spinal cord?
What is this syndrome called?

A
  1. loss of fine touch, proprioception, vibration ipsilateral to the lesion
  2. loss of pain, temperature contralateral to the lesion

Brown- Sequard syndrome

44
Q

If there is injury to sensory axons above the medulla, what will be the presentation?

A

Contralateral loss of fine touch, proprioception, vibration, pain and temperature because the medial leminiscus has already crossed to contralateral side at this point.

45
Q

What are the 4 major visual systems?

What does each allow for?

A
  1. retino-geniculo-calcarine pathway [visual perception at a conscious level]
  2. pupillary light reflex [bilateral connections via pretectal and EW nuclei in the midbrain]
  3. rapid, reflexive responses [superior colliculi in the midbrain]
  4. circadian rhythms [hypothalamus connection]
46
Q

If there is a lesion in the eye or optic nerve, what is the result?

A

monocular blindness on the same side of the lesion

47
Q

If there is a lesion in the optic chiasm, what is the result?

A

Bitemporal hemianopsia [peripheral vision is blocked]

48
Q

If there is a lesion in the optic tract or lateral geniculate nucleus, what is the result?

A

contralateral homonymous hemianopsia

[if the lesion is on the left lateral geniculate, you will lose the medial vision of the left eye and the lateral vision of the right eye]

49
Q

If there is a lesion in the inferior optic radiation [temporal lobe], what is the result?

A

contralateral superior quadrantanopsia

[if you knock out left inferior optic radiation, you will lose the right upper quadrant of both eyes]

50
Q

If there is a lesion in the right superior optic radiation [parietal lobe] what is the result?

A

contralateral inferior quadrantanopsia

[left lower quadrant is knocked out in both eyes]

51
Q

If there is a lesion in the medial occipital cortex/white matter, what will be the visual outcome?

A

contralateral homonymous hemianopsia but with macular sparing

52
Q

Describe the direct loop of basal ganglia initiated movement.

A
  1. D1 neurons in the putamen are activated by dopamine
  2. D1 acts on globus pallidus medial [GPM] increasing inhibition
  3. GPM is inhibited so it exerts LESS inhibition on the thalamus
  4. Since the thalamus is not inhibited, it can increase stimulation of the cerebral cortex [motor]
53
Q

Describe the indirect loop of basal ganglia.

A
  1. D2 on putamen is inhibited by dopamine
  2. This releases inhibition of globus pallidus externa
  3. GPL is not able to inhibit STN as much
  4. STN excites substantia Nigra reticulata
  5. SNr inhibits the thalamus
  6. decreased cortical activity
54
Q

What is the overall effect of the direct and indirect basal ganglia loops on movement/cortical stimulation?

A

Direct- stimulates cerebral cortex by increasing thalamic firing

Indirect- decreases activity of thalamic neurons and decreases cortical activity

55
Q

What is the effect of a stroke that injures the contralateral STN?

A

Hemiballism because the STN usually activates the SNr to inhibit the thalamus.
No STN, no SNr, uncontrolled thalamic firing.

56
Q

What are the 8 possible sites of neurologic disease from most central to most peripheral?

A
  1. cortex
  2. subcortical white matter/gray matter
  3. brainstem
  4. spinal cord
  5. anterior horn cells
  6. peripheral nerve
  7. NMJ
  8. muscle
57
Q

Is localization of lesions more precise in peripheral or central sites? Why?

A

Localization is more precise when it involves peripheral sites because they signs/symptoms are restricted and do not change much over time

58
Q

Define paresis and plegia.

A
Paresis = weakness
Plegia = paralysis
59
Q

What terms describe:

  1. weakness in one limb
  2. weakness on one side of the body
  3. weakness in the lower extremities
  4. weakness in the upper limbs
  5. weakness of all 4 limbs
A
  1. monoparesis or monoplegia
  2. hemiparesis or hemiplagia
  3. paraparesis or paraplegia
  4. brachial diplegia or diparesis
  5. quadraparesis or quadraplegia
60
Q

What is the difference between UMN and LMN?

A

UMN- descending motor system in brain and spinal cord

LMN - anterior horn cells, nerve roots [ventral and dorsal], NMJ, muscle fiber]

61
Q

What cells are susceptible to:

  1. ALS
  2. poliomyelitis
  3. Guillan-Barre
  4. Myasthenia Gravis
A
  1. anterior horn cells
  2. anterior horn cells
  3. peripheral nerves and possibly nerve root
  4. NMJ
62
Q

When assessing strength, a patient with lesions in which 2 areas would present either normally or with hemiparesis?
Which patients would present with weakness?
Which patients would present with proximal weakness?

A

Normal/hemiparesis = brain or spinal cord

Weakness=
anterior horn cell, peripheral nerve, MMJ

Proximal weakness = muscles

63
Q

You are assessing a patient and they have normal to increased DTR. They demonstrate an extensor plantar response. What 2 locations could the lesion be in?

A

Brain or spinal cord

64
Q

When assessing DTR, lesions in what 2 areas would cause weak or absent DTR?

A

Decreased DTR in:

  1. anterior horn cells
  2. proximal nerves
65
Q
When assessing DTR, which lesions would :
1. increase
2. decrease
3. not change 
the DTR?
A

Increase : brain and spinal cord
Decrease : anterior horn cells and proximal nerves
No change: NMJ and muscle

66
Q

You are assessing a patient and notice fasciculations. A patient with a lesion in what area would have:

  1. prominent fasciculations
  2. probable fasciculations
A

Prominent in anterior horn cells

Possible in peripheral nerve

67
Q

A older woman presents with:

  1. mild hemiparesis
  2. increased DTR and extensor plantar response
  3. no fasciculations
  4. normal/slightly atrophic muscles from disuse
  5. normal–> slight lack of sensation.

What are the 2 possibilities of where the lesion could be and what is are the likely causes?

A

Brain lesion - CVA/stroke

Spinal cord- myelitis

68
Q

A patient presents with:

  1. weakness
  2. decreased/absent DTR
  3. prominent fasciculations
  4. prominent proximal atrophy
  5. normal sensation

Where is the lesion most likely to be and what are 2 possible causes of this?

A

Anterior horn cells

  1. ALS
  2. Poliomyelitis
69
Q

A patient presents with:

  1. weakness
  2. decreased/absent DTR
  3. possible fasciculations
  4. DISTAL atrophy of muscle mass
  5. sensory loss

Where is the likely lesion?

A

Peripheral nerve

*** only location with muscle AND sensory loss

70
Q

A patient presents with:

  1. weakness
  2. normal DTR
  3. no fasciculations
  4. normal muscle mass
  5. normal sensation

What is the likely location of the lesion?

A

NMJ = myesthenia gravis

71
Q

A patient presents with:

  1. weakness [proximal]
  2. normal DTR
  3. no fasciculations
  4. proximal atrophy with distal pseudohypertrophy
  5. normal sensation

Where is the likely lesion?

A

muscle - myopathy

72
Q

A patient presents with sensory loss and dysesthesia [altered pain perception] involving:

  1. entire body on one side
  2. face on the ipsilateral side to the lesion

Where would the likely lesion be?

A
  1. Postcentral gyrus [primary somatosensory gyrus]

2. thalamic lesion

73
Q

A patient presents with facial numbness and contralateral body numbness. Where is the likely lesion?
What other symptoms would you be likely to see?

A

This lesion is probably in the brainstem and you would be likely to see signs/symptoms associated with:

  1. motor tracts
  2. CNs
74
Q

Where is the lesion if there is loss of pain and temperature with preservation of vibration and position sense?

A

Anterior spinal cord

75
Q

Where is the lesion if there is loss of vibration and proprioception ipsilateral to the lesion and pain and temperature contralateral to the lesion?

A

hemi-cord [Brown-Sequard]

76
Q

Where is the lesion if there is loss of proprioception, vibration and fine touch on both sides of the body with no other motor or sensory deficits?
What disease is likely to present in this way?

A

This means that the dorsal column was knocked out which is common for tertiary syphilis [tabes dorsalis]

77
Q

You are examining a patient and notice loss of pain and temperature sense on both sides. This patient also has bilateral weakness, with prominent fasciculations. The DTR is decreased and there is prominent proximal atrophy of muscles. What is the likely lesion?

A

Anterior Spinal Artery syndrome

  • loss of pain temp from anterolateral tract
  • preserved vibration/proprioception
  • messed up anterior horn cells
78
Q

A patient presents with loss of proprioception and vibration bilaterally. They also have increased DTR, normal strength to slight hemiparesis, no fasciculations, normal muscle mass.
What is the likely cause of the problem?

A

This shows a lesion in the dorsal column AND lateral corticospinal tract.
This is associated with “subacute combined system degeneration” due to a lack of B12.

79
Q

What is aphasia and what is the most common cause?

What are the 3 main types ?

A

It is an impairment of language and speech that affects the production or comprehension of speech and the ability to read/write.

Most common cause is a stroke.

  1. receptive aphasia [wernickes]
  2. conduction aphasia [arcuate fasciculus]
  3. expressive aphasia [broca’s]
80
Q

A patient presents to you and they don’t seem to be understanding what you are saying to them. They are able to fluently speak but the words are nonsensical and it is difficult to comprehend the person.
They are not able to name objects or repeat phrases.
What does this person have and most likely what was the cause?

A

Wernicke’s aphasia - most likely caused by an embolic stroke in the left superior temporal lobe.

81
Q

A patient presents with agrammatism, anomia, and articulation difficulties. His speech is slow and full of pauses. He is frequently mispronouncing words.
The person is aware of the difficulity he is having because he has comprehension.
What is the problem and likely cause?

A

Broca’s aphasia often caused by a left middle cerebral artery ischemic stroke

82
Q

A patient presents and they are able to comprehend what you are saying. They are also able to speak fluently, however, they struggle with repetition and naming. Where is the likely problem?

A

Conduction aphasia - problem with the arcuate fasciculus

83
Q

An elderly gentleman on your service is showing significant distractibility and inattention. His thought process is slow and he is not concentrating.
The symptoms of impaired consciousness seem to wax and wane.
What does he most likely have?
What are common causes of this?

A

Delerium- acute confusional state

Causes:

  1. infections
  2. metabolic disorders
  3. nutritional disorders
  4. CNS insult
  5. drugs/meds
83
Q

An elderly gentleman on your service is showing significant distractibility and inattention. His thought process is slow and he is not concentrating.
The symptoms of impaired consciousness seem to wax and wane.
What does he most likely have?
What are common causes of this?

A

Delerium- acute confusional state

Causes:

  1. infections
  2. metabolic disorders
  3. nutritional disorders
  4. CNS insult
  5. drugs/meds
84
Q

A woman comes to see you. Her daughter tells you she has been progressively declining in memory and cognitive function.
What does she most likely have? What area of the brain is likely affected? Is this process reversible?

A

Dementia- insidious and progressive process that cannot be stopped. It tends to affect certain brain areas [hippocampus, frontal lobe etc] so the level of consciousness is normal initially.

84
Q

A woman comes to see you. Her daughter tells you she has been progressively declining in memory and cognitive function.
What does she most likely have? What area of the brain is likely affected? Is this process reversible?

A

Dementia- insidious and progressive process that cannot be stopped. It tends to affect certain brain areas [hippocampus, frontal lobe etc] so the level of consciousness is normal initially.

85
Q

How do delerium and dementia differ in terms of:

  1. level of consciousness
  2. course
  3. autonomic hyperactivity
  4. prognosis
A

Delerium has impaired consciousness, acute/fluctuating course, hyperactivity and is reversible.

Dementia is normal consciousness [until late], progressive steady course, no hyperactivity, irreversible

85
Q

How do delerium and dementia differ in terms of:

  1. level of consciousness
  2. course
  3. autonomic hyperactivity
  4. prognosis
A

Delerium has impaired consciousness, acute/fluctuating course, hyperactivity and is reversible.

Dementia is normal consciousness [until late], progressive steady course, no hyperactivity, irreversible

86
Q

What are the 2 categories of seizures?

A
  1. Generalized seizure- all the brain has abnormal electrical discharge at the same time
  2. Partial seizure- focal area of the brain [signs/symptoms depend on what area of the brain is involved]
86
Q

What are the 2 categories of seizures?

A
  1. Generalized seizure- all the brain has abnormal electrical discharge at the same time
  2. Partial seizure- focal area of the brain [signs/symptoms depend on what area of the brain is involved]
87
Q

A patient starts with an aura of fear, nausea and tingling. Then consciuosness becomes impaired and they look dazed.
Next there is repetitive movements.
This lasts 1-5 minutes after which the patient appears drowsy.
What just happened?

A

Complex partial seizure

[differs from simple because

87
Q

A patient starts with an aura of fear, nausea and tingling. Then consciuosness becomes impaired and they look dazed.
Next there is repetitive movements.
This lasts 1-5 minutes after which the patient appears drowsy.
What just happened?

A

Complex partial seizure

[differs from simple because in simple the patient does not have altered consciousness]

88
Q

What 3 classes of neurological insults can cause coma?

A
  1. Supratentorial - large lesions that affect both hemispheres and/or encroach on diencephalon
  2. subtentorial - small direct damage to arousal centers in the brainstem
  3. toxic/metabolic- diffuse dysfunction of neurons throughout the brain
89
Q

A patient presents with waxing and waning of arousal. Their neuro exam is symmetric. They have deep, rapid respirations. The pupils are symmetrically small with preserved reactivity. They have roving spontaneous eye movements with full excursion.
What does this person likely have?

A

A toxic/metabolic coma

90
Q

A patient presents with a low level of arousal. They seem to be progressively deteriorating. Breath is normal.
On fundoscopic exam, you note papilledema.
The pupils are asymmetric and there is asymmetry to the movement of the eyes.

What is the likely cause?

A

Structural coma.

91
Q

Papilledema usually does NOT occur with toxic/metabolic coma. What are 3 exceptions?

A
  1. hypoparathyroidism
  2. lead intoxication
  3. malignant hypertension