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(YEAR 1) PBLs > Brain and Behaviour PBL: Brainstem Tumour > Flashcards

Brain and Behaviour PBL: Brainstem Tumour Flashcards

1
Q

What is intracranial hypertension?

A

Increased pressure inside the skull which can cause compression of blood vessels, nerves or brain tissue itself which can inflict permanent damage

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2
Q

What is the fundus of the eye?

A

Interior surface of the eye opposite the lens, and includes the retina, optic disc, macula, fovea and posterior pole

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3
Q

What is ataxia?

A

Llack of muscle coordination which may affect speech, eye movements, the ability to swallow, walking, picking up objects and other voluntary movements. A person with persistent ataxia may have damage in the part of the brain that controls muscle coordination - the cerebellum.

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4
Q

What is the optic disc?

A

the raised disc on the retina at the point of entry of the optic nerve, lacking visual receptors and so creating a blind spot

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5
Q

What is the fovea centralis?

A

a small depression in the retina of the eye where visual acuity is highest

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6
Q

What is the macula lutea?

A

an oval yellowish area surrounding the fovea near the centre of the retina in the eye, which is the region of keenest vision

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7
Q

What is the sclera?

A

the white outer layer of the eyeball. At the front of the eye it is continuous with the cornea

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8
Q

What is the ciliary body?

A

the part of the eye that connects the iris to the choroid; consists of ciliary muscle, ciliary process and ciliary ring

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9
Q

What is the iris?

A

a flat, coloured, ring-shaped membrane behind the cornea of the eye, with an adjustable circular opening (pupil) in the centre

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10
Q

What is the cornea?

A

the transparent layer forming the front of the eye

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11
Q

What is choroid?

A

the pigmented vascular layer of the eyeball between the retina and the sclera.

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12
Q

Describe the physiology of the accommodation reflex

A
  1. Optic nerve afferents (CN II) travel to lateral geniculate nucleus (LGN)
  2. The optic nerve afferents –> primary visual cortex (occipital lobe)
  3. Some fibres from occipital lobe go to the cells of accommodation centre (midbrain) near the pre-tectal region
  4. From here;fibres travel from the accommodation centre to EW nucleus
  5. At EW nucleus parasympathetic stimulation occurs –> ciliary muscle contraction –> shortens the suspensory ligament –> lens relaxation and passive thickening
  6. Accommodation centre also stimulates oculomotor efferents –> medial rectus –> convergence of the eyes to a near object
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13
Q

Describe the physiology of the pupillary light reflex

A
  1. Light activates retinal afferents of optic nerve (CN II) –> pretectal nuclei (just in front of the superior colliculus)
  2. Axons from the pretectal nuclei –> Edinger Westphal nuclei and the contralateral connection crosses in the posterior commissure before synapsing in the EW nuclei
  3. Preganglionic fibres (parasympathetic) from the EW enter the oculomotor nerve (CN III) and synapse in the ciliary ganglion
  4. Postganglionic fibres innervate the constrictor muscle of the iris (sphincter pupillae) –> pupillary constriction
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14
Q

What are the types of brainstem glioma?

A

Diffuse intrinsic pontine glioma and focal/low grade glioma

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15
Q

What is a risk factor for the development of a brainstem tumour?

A

Neurofibromatosis type 1

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16
Q

What are the symptoms of a brainstem glioma?

A

Loss of balance, Unilateral motor loss Headache, Nausea and vomiting, Unusual sleepiness, Vision/hearing problems, Behaviour changes, Learning issues

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17
Q

What is a diffuse intrinsic pontine glioma (DIPG)?

A

Fast growing tumour which spreads all throughout the brainstem and is difficult to treat and has a poor prognosis

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18
Q

What is a focal/low grade glioma?

A

Slow growing tumour which is in one area of the brainstem, making it easier to treat and have a better prognosis (than DIPG)

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19
Q

How is physical exam and history used in the diagnosis of a brainstem glioma?

A

check general health, look for lumps or anything else unusual as well as taking notes on the patient’s health habits and whether they have any previous disease history.

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20
Q

How is neurological exam used in the diagnosis of a brainstem glioma?

A

used to assess the brain, spinal cord and nerve function by checking mental status, coordination, gait and how motor, sensory and reflexes work.

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21
Q

How is an MRI with gadolinium used in the diagnosis of a brainstem glioma?

A

through the use of a magnet, radio waves and a computer when gadolinium is injected into a vein (collects around cancer cells to brighten appearance in image). Procedure also known as nuclear magnetic resonance imaging.

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22
Q

How is a biopsy used in the diagnosis of a brainstem glioma?

A

If the MRI scan looks like the tumor is a DIPG, a biopsy is usually not done and the tumor is not removed. However, if it looks like focal or low-grade brain stem glioma a part of the skull is removed and a needle is used to remove a sample of the brain tissue; if cancer cells are found, the doctor will remove as much tumor as safely possible during the same surgery.

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23
Q

Describe internal radiation therapy in brainstem glioma treatment

A

Involves using a radioactive substance sealed in needles/seeds/wires/catheters which are then placed directly into or near the cancer

24
Q

Describe external radiation therapy in brainstem glioma treatment

A

Uses a machine outside the body to send radiation towards the cancer.

25
Q

Describe conformational radiation therapy in brainstem glioma treatment

A

Uses a computer to make a 3D image of the tumour and then shapes the radiation beams to fit the tumour in order to supply a high dose of radiation which causes less damage to normal tissue around the tumour.

26
Q

Why may chemotherapy be preferential over radiation therapy in the treatment of tumours in children?

A

Radiation therapy can affect growth and brain development in young children

27
Q

Describe chemotherapy in brainstem glioma treatment

A

Either kills or stops cancer cells from dividing, as is either given systemically (blood stream) or regionally (CSF)

28
Q

Describe cerebrospinal fluid diversion in brainstem glioma treatment

A

This is used to drain fluid build-up in the brain by inserting a long, thin tube (shunt) into a ventricle of the brain, and then threaded to another part of the body e.g. abdomen where the fluid drains is reabsorbed, in order to relieve pressure.

29
Q

Describe targeted therapy in brainstem glioma treatment

A

The use of drugs to identify and attack specific cancer cells, though these are in early days.

30
Q

What is the prognosis for DIPG tumours?

A

Very poor, 90-100% of patients dying within 2 years of diagnosis

31
Q

What is the prognosis for focal/tectal gliomas?

A

Excellent long-term survival with CSF shunting

32
Q

Describe the DCML tract

A
  • Ascending (sensory) pathway
  • Contralateral deficits above medulla
  • Carries information about proprioception (joint sense) and discriminative touch
  • Decussation: secondary afferents decussate at the medulla after the primary afferents synapse in the gracile/cuneate nuclei
33
Q

What is the role of the gracile fasciculus?

A

Carries information from lower body

34
Q

What is the role of the cuneate fasciculus?

A

Carries information from upper body

35
Q

Describe the spinocerebellar tract

A
  • Ascending (sensory) pathway
  • Ipsilateral deficits
  • Carries information about non-conscious and unconscious proprioception to the cerebellum
  • Decussation: first at the level of spinal entry, and then again in the pons
36
Q

Describe the spinothalamic tract

A

•Ascending (sensory) pathway
•Contralateral deficits
•Carries information about crude touch, pain and temperature
oAnterior tract = pressure and passive touch
oLateral tract = pain and temperature
•Decussation: at the level of spinal entry

37
Q

Describe the corticospinal tract

A

•Descending (motor) pathway
•Contralateral deficits
•Carries action potentials to voluntary muscles movement
•Decussation: mainly at the spino-medullary junction (pyramids)
oVentral corticospinal tract doesn’t decussate until spinal level
oLateral corticospinal tract decussates at the spino-medullary junction

38
Q

What cranial nerve nuclei are within the pons?

A

V,VI,VII,VIII (trigeminal, abducens, facial, vestibulocochlear)

39
Q

What cranial nerve nuclei are within the medulla?

A

IX,X,XI,XII (glossopharyngeal, vagus, spinal accessory, hypoglossal)

40
Q

Which cranial nerve nuclei are within the midbrain?

A

III, IV (oculomotor and trochlear)

41
Q

Explain why the individual with DIPG presents with diplopia

A

Abducens nerve nuclei in the pons compressed; nerve usually innervates lateral rectus muscle which abducts the eye, therefore they can’t move their right eye to the right –> visual input not synchronised –> double vision

42
Q

Explain why the individual with DIPG presents with a medially deviated right eye which can’t abduct

A

Compression of abducens nerve nuclei as the paralysis of the lateral rectus muscle means the action of the medial rectus muscle is unopposed –> medial deviation, and lateral rectus cannot facilitate abduction

43
Q

Explain why the individual with DIPG presents with a right-side facial droop

A

Facial nerve nuclei are within the pons; usually responsible for innervating the muscles of facial expression, so paralysis –> paralysis of ipsilateral side

44
Q

Explain why the individual with DIPG presents with right-side facial numbness

A

Trigeminal nerve nuclei are within the pons; sensory innervation to the face, so this is likely to be compressed

45
Q

Explain why the individual with DIPG presents with unsteadiness when walking

A

Corticopontine fibres from primary motor cortex –> ipsilateral pontine nucleus (ventral pons) –> pontocerebellar projection carries that information to the contralateral cerebellum via middle cerebellar peduncle.Therefore damage to the pontocerebellar project disrupts the communication of information to the cerebellum about movement (which works to coordinate motion)

46
Q

As DIPG progresses, why may the individual present with headaches, nausea and vomiting?

A

Increased intracranial pressure –> irritation of dura –> sensitive to pain, especially at dural venous sinuses and meningeal arteries –> trigeminal (V) sensory afferents –> sensation of pain
OR
Double vision and inability to focus on an object –> eye strain –> headache

47
Q

As DIPG progresses, why may the individual present with blurred vision?

A

Blurred vision is likely to result from compression of the oculomotor nerve as the tumour progresses superiorly into the midbrain as this nerve is involved in altering the lens thickness by innervating the ciliary muscles of the eye (accommodation reflex)

48
Q

As DIPG progresses, why may the individual present with intracranial hypertension?

A

Likely to be due to the tumour compressing the ventricles of the brain, and causing the displacement of the CSF, causing it to fill up any available space and subsequently increasing the pressure inside the head.

49
Q

As DIPG progresses, why may the individual present with ataxia?

A

As the tumour progresses inferiorly, it will compress/damage the remaining fibres going to and from the cerebellum to the brainstem; reticulocerebellar fibres (pons), olivocerebellar fibres (medulla) and vestibulocerebellar fibres (medulla), so that it can elicit no coordination over the movements of the body.

50
Q

As DIPG progresses, why may the individual present with weak limbs and hyper-reflexia?

A

Upper motor neurone damage to the corticospinal tract which decussates in the pyramids of the medulla, hyper-reflexia at level of lesion

51
Q

As DIPG progresses, why may the individual present with hearing loss in the right ear?

A

Tumour is compressing on the vestibulocochlear nerve, preventing the transmission of auditory information (cochlear portion) - this is in the pons (sensory neurones are more lateral, motor neurones are more medial)

52
Q

As DIPG progresses, why may this cause loss of consciousness and death?

A

The brainstem has many vital roles, not least: cardiovascular system, respiratory, alertness, awareness and consciousness, and therefore damage leads to death often

53
Q

Explain why chemotherapy cannot be used in the treatment of DIPG

A

Chemotherapy is often used as part of a clinical trial in the treatment of DIPG in an attempt to improve survival, however, its use has never demonstrated a significant improvement in the outcome beyond that achieved by radiation alone

54
Q

Explain why surgery cannot be used in the treatment of DIPG

A

Surgery cannot be used as the tumour will be spread throughout the brainstem, so likely to cause more damage.

55
Q

What is ataxia?

A

the loss of full control of bodily movements

(YEAR 1) PBLs (29 decks)

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