Case 16- Headaches and Safeguarding Flashcards
(76 cards)
1
Q
How do you classify headaches
A
- Primary headache- 90% of headaches, headaches is the main problem, episodic and benign
- Secondary headache- another condition is causing the headache, can be benign but also life threatening
2
Q
Examples of primary and secondary headaches
A
- Primary headache- tension-type, migraine, cluster headache, other
- Secondary headaches- substances/withdrawal, head, neck and ENT, homeostatic dysfunction, psychiatric, vascular, space occupying lesion, raised intracranial pressure, subarachnoid haemorrhage, meningitis and encephalitis, cerebral venous sinus thrombosis, giant cell arteritis, acute angle closure glaucoma and intracranial infection.
3
Q
Tension type headache
A
Most common type, common in young adults. Can be associated with stress and depression. There are two types, Episodic: <15 days per month and Chronic: >15 days per month. Usually no other symptoms, will have a normal neurological exam. Mild/moderate, bilateral pain like a tight band squeezing around your head. May also have neck pain, can get radiation from neck to head. Some are associated with cervical spondylosis. Varying duration from 30 minutes to 7 days.
4
Q
The three main types of migraines
A
- Migraine without aura
- Migraine with aura
- Migraine aura without headache
5
Q
Types of aura’s
A
- Visual aura- flashes of light, temporary vision, visual hallucinations
- Sensory aura- tingling, numbness
- Motor aura- weakness or paralysis on one side of the body
6
Q
Migraines
A
Affects 1 in 7 people, can have a huge impact on patient quality of life. Usually starts in childhood/young adulthood. More common in women. The triggering event causes activation of the trigeminovascular pathways causing a migraine. The headache is usually a unilateral throbbing sensation, they may have nausea, vomiting, photophobia and noise sensitivity.
7
Q
The 4 phases of a migraine
A
- Prodrome- symptoms experienced before the headache
- Aura- transient focal neurology symptoms which usually precede the headache
- Headache- usually 1 hour after the aura
- Postdrome- symptoms after the headache, usually lethargy
8
Q
Migraine triggers
A
Alcohol, Smell, Foods, Medication, Sounds, Lights, Lack of sleep, Caffeine, Weather, Hereditary predisposition, Stress and Skipped meals.
9
Q
When should you take medication for a migraine
A
It needs to be taken as early in the headache phase as possible
10
Q
What guides acute management of headaches:
A
- Patient’s preference
- Response to previous treatment
- Frequency and severity of headaches
- Co-morbidities
11
Q
When should you take medication for a migraine (MOH)
A
Medication is limited to two days a week, it reduces the risk of medication overuse headaches (MOH). MOH may be a factor in up to 50% of people with chronic headaches. Its seen when patients overuse headache medication (10-15 days per month for a period of 3 months).
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Q
Cluster headache
A
A rare type of primary headache, more common in males. Between the ages of 20-40, more common in smokers. Tends to occur in bouts and then remit over months/years- hence cluster. If its episodic the remission period is more then a month, if its chronic then there is no remission period or its shorter. There is variation on classification between the two.
13
Q
Features of a cluster headache
A
- Features: severe unilateral pain around the eye (periorbital/temporal area)
- Associated with ipsilateral autonomic symptoms- Eye watering, nasal congestion, rhinorrhoea, facial sweating, eyelid swelling
- Excruciating, sharp (not pulsatile) pain which is usually behind the eye
- Known as the ‘suicide headache’ – it is very severe and causes patients a lot of distress
- Lasts 15 minutes to 3 hours
- Typically occurs at night and wakes the patient from sleep- red flag symptoms
- Rapid onset
- Not associated with auras or nausea/vomiting
14
Q
Less common primary headaches
A
- Primary cough headache
- Primary sexual headache
- Primary stabbing headache
- Primary thunderclap headache
- Primary hypnic headache
- Hemicrania continua
15
Q
Key facts tension-type headache
A
Timing= 30min-7 days
Character= Squeezing, tight band
Triggers= Stress, anxiety
Impact= may cause patients to reduce daily activities
Health between attacks- well between attacks
16
Q
Key facts- Migraines
A
Timing= 4h- 3 days
Character= Unilateral, Pulsating
Triggers= lack of/too much sleep, chocolate, cheese, premenstrual, missed meals, dehydration
Impact= significant impact, may need to sleep during attacks. Aggravated by physical activity
Health between attacks- well between attacks
17
Q
Key facts- cluster headaches
A
Timing= 5m- 3h
Character= Unilateral, behind the eye, sharp, constant
Triggers- Alcohol, lack of sleep
Impact- significant impact during cluster bouts
Health between attacks- well between attacks
17
Q
Key facts- cluster headaches
A
Timing= 5m- 3h
Character= Unilateral, behind the eye, sharp, constant
Triggers- Alcohol, lack of sleep
Impact- significant impact during cluster bouts
Health between attacks- well between attacks
18
Q
What is needed to diagnosed a secondary headache
A
When all 3 criteria are met:
• When we find evidence of a condition known to cause a headache
• The headache corresponds in timing with the condition we have found
• The headache resolves if we treat the underlying disorder
19
Q
Dangerous and non-dangerous secondary headaches examples
A
- Not-immediately life threatening- substance/withdrawal of substances, head, neck and ENT, Homeostatic dysfunction, Psychiatric
- Dangerous- vascular, raised intracranial pressure, intracranial infection, space occupying lesion, inflammatory
20
Q
Vascular causes of secondary headaches- Subarachnoid haemorrhage (SAH)
A
Bleeding into the subarachnoid space (between the pia and arachnoid matter). The bleeding suddenly increases the intracranial pressure and the blood also has an irritant effect on the brain and cerebral vessels.
21
Q
Commonest cause of non-traumatic SAH
A
Ruptured berry (sacular aneurysm)
• Berry aneurysms tend to grow in the circle of Willis
• Berry aneurysms have an association with Polycystic kidney disease
22
Q
Causes of a berry aneurysm
A
- Genetic- Marfan’s, Ehlers-Danlos
- Arteriovenous malformations
- Trauma- moderate to severe injury
- Infections- cause weakness in vessels
- Smoking, hypertension, alcohol excess
23
Q
Clinical presentation of a SAH
A
- Presents as explosive headache or ‘thunderclap headache’- worst ever (red flag). Like being hit on the head with a bat
- Reaches peak intensity within 3 seconds but any headache that peaks in less then a minute should make you worried
- Occipital- usually but not always
- Mean age of 50
- May have signs of meningism- headache, neck stiffness, photophobia
- Nausea and vomiting
- If severe- leads to raised intracranial pressure and reduced consciousness
- Sentinel bleeds- multiple less severe headaches from aneurysms leaking. When only one aneurysm ruptures it’s a thunderclap headache
- High mortality and morbidity- an important not to miss diagnosis, reduced consciousness and neurological signs indicate worse prognosis
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Heaches- causes of raised intracranial pressure
* Space occupying lesions i.e. tumour, abscess
* Intrancranial infections i.e. meningitis, encephalitis
* Disturbance of CSF flow
* Bleeds/head trauma i.e. SAH, subdural
* Idiopathic
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Clinical presentation of raised intracranial pressure
* Triad of headache, vomiting and papilledema (swelling to the optic disc- red flag symptom seen on fundoscopy)
* Headache- gradual onset, worse in the morning (red flag) and coughing, wakes from sleep (red flag)
* Visual disturbances (red flag)
* Changes in mental state (red flag)- caused by distortion of the upper brainstem leading to reduced consciousness
* Late signs- raised BP, wide pulse pressure, bradycardia (Cushing’s triad), caused by compression of the medulla
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Space occupying lesion (SOL)
* A cause of raised intracranial pressure
* Normally a tumour, 50% of tumours are primary brain tumours. May also be an abscess or haematoma.
* SOL produces signs and symptoms by 3 mechanisms: directly- pressing on other structures, by raising intracranial pressure around the brain, by provoking seizures- the lesions make the brain more unstable
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Red flags that indicate a high risk of a space occupying lesion
* New headache in a patient with a history of cancer or immunosuppression
* Headache and focal neurology
* Worsening headache- may indicate something is growing within the brain
* Headaches associated with seizures
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Headaches- types of intracranial infection
• Meningitis- inflammation of the meninges
• Encephalitis- inflammation of the brain
• Meningoencephalitis- both inflammation of the brain and the meninges
Its usually caused by an infection though there are non-infective causes of meningitis and encephalitis
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Temporal arteritis (giant cell arteritis)
* Inflammation of the arteries
* Common in the elderly
* Presentation- headache, temporal artery and scalp tenderness (i.e. when combing hair), tongue/jaw claudication. May have general symptoms; flu-like, unintentional weight loss, depression and tiredness
* Risk of irreversible bilateral visual loss, which can occur suddenly if not treated
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Non-life threatening secondary headaches
* Substances/withdrawal of substances
* Head, neck, ENT- sinusitis, temporomandibular joint disorder, dental problems, ear pathology
* Homeostatic dysfunction- fasting, obstructive sleep apnoea (due to hypercapnia)
* Psychiatric- somatisation, recurrent and frequently changing physical symptoms
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Antimigraine drugs- Analgesia
* Simple analgesia- i.e. NSAIDs (aspirin, ibuprofen), paracetamol
* Usually orally but can be done rectally if the patient is vomiting i.e. Diclofenac
* Should be taken at the start of the headache phase as patients often get gastric stasis which impairs drug absorption
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Antimigraine drugs= Anti-emetics
* For example- cyclizine, metoclopramide are helpful in conjunction with analgesia
* Can be given orally or parentally depending on whether the patient is vomiting
* Patients can get gastric stasis which impairs drug absorption. Some anti-emetics are pro-kinetic (i.e. metoclopramide) and increase gastic emptying- this helps to prevent gastric stasis and improve drug absorption.
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Anti-migraine drugs Triptans
* 5HT1 receptor agonists i.e. sumatriptan, zolmitriptan, rizatriptan
* Can be given orally, subcutaneously (injection) or as a nasal spray
* Should be used during the headache phase not aura
* Avoid using for more then 10 days per month
* Theory that migraine is caused by vasodilation- triptans cause vasoconstriction if intracranial blood vessels
* Inhibits the abnormal activation of peripheral nociceptors
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First line treatment for migraines- combination therapy
• Oral triptan + NSAID (most effective)
• Oral triptan + paracetamol (if NSAID contraindicated)
Consider oral antiemetic – even in the absence of N&V
Can consider monotherapy if that’s patient’s preference. Either triptan, NSAID, high-dose aspirin or paracetamol on its own depending on patient
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When should you consider prophylaxis
* Significant impact
* Migraine is not responding to acute treatment
* Person is at risk of a medication overuse headache
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Migraine prophylaxis
* Topiramate = anti-epileptic medication. Associated with fetal malformations in pregnancy. Ensure highly effective contraception if required
* Propanolol = beta-blocker
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Other options for migraine prophylaxis
If first line is not suited/tolerated
• Amitriptyline(antidepressant)
• Riboflavin (vitamin B2)
• Non-pharmacological e.g. acupuncture, mindfulness
Migraine that doesn’t respond to pharmacological prophylaxis - Botulinum toxin type A (specialist treatment)
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The principaks of safeguaring as defined by the care act 2014
- Accountability = adequate training + knowledge
- Empowerment = supporting + encouraging victims
- Partnership = working with MDT
- Prevention = take action before harm
- Proportionality = assessment of risk
- Protection = being an advocate
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Toxic triad
1) Mental health
2) Domestic violence
3) Substance abuse
Its seen in a lot of child safeguarding situations, when these factors exist you should consider the safety of the child
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Family/environmental factors for abuse
* Domestic abuse
* Substance abuse
* Mental health
* Lack of parenting skill
* Social deprivation
* Stress at home
* Violent offhanding
* Vulnerable / unsupported carers
* Previous child maltreatment
* Who lives at home?
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Child factors for abuse
Age (young), child carers, disability, absent from education, criminal or antisocial behaviour, missed appointments, living in care system, running away, frequent attendance at hospital/healthcare.
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Presentation of child abuse
* Inconsistent history
* Late presentation
* Development incongruity
* Injuries in unusual sites
* Prescence of other injuries / repeated injuries
* Behavioural changes
* Sexualised behaviour
* Unplanned pregnancy/ STI
* Very young girls attending for contraception
* Bullying
* Unkempt
* Dental caries
* Withdrawn/fearful
* Lack of interaction between carer and child
* Worsening mental health
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Why do get doctors get safeguarding wrong
* Lack of information about the child and family
* No time to deal with it
* Lack of context (only seeing a snapshot)
* Lack of knowledge on how to spot and deal with safeguarding concerns
* Not even considering it
* Assuming the best of people
* Assumptions about groups who are more or less likely to be affected
* Own issues/memories
* Fear of consequences for the child/family
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Meninges
1) Membraneous covering of the brain and spinal cord.
2) They have a supportive role by providing a framework for the cerebral and cranial vasculature.
3) Provide protection to the CNS from mechanical damage alongside the CSF.
4) The most superficial layer is the dura mater, then the arachnoid mater and pia mater.
5) The arachnoid mater has extensions called trabeculae which join to the pia mater.
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Dura mater
1) Tough, fibrous membrane that covers the spinal cord and the brain.
2) Loose.
3) It’s a double membrane within the cranium.
4) There is an outer Periosteal layer and an inner Meningeal layer.
5) The layers mostly adhere to each other but in certain regions they separate to form dural reflections and venous sinuses.
6) The extra-dural space is between the bone and dura mater and is a potential space. In the craium the dura is adherent to the bone.
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Dura mater in the spinal cord
The meningeal layer exists the skull and forms a protective layer of the spinal cord. The Periosteal layer of the dura becomes the outer Periosteum. So within the spinal cord the dura mater is only made of one layer. In the spinal cord the dura mater is separate from the bone, so the extra-dural space forms.
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Dural reflections
Separation of the two dural layers. Extends into the fissures of the brain, provides support
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Examples of dural reflections
* Falx cerebri- in the great longitudinal fissure which divides the two cerebral hemispheres
* Tentorium cerebelli- transverse fissure, between the occipital lobe and the cerebellum
* Falx cerebelli- between the cerebellum lobes
* Diaphragma sellae- covers the hypophyseal fossae, where the pituitary gland is sitting
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The Leptomeninges
* Arachnoid- thin, avascular, lines the dura but does not adhere, loose fitting around the brain
* Pia mater- thin, translucent, tightly adherent to the surface of the brain, follows the gyri and sulci
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The Subdural space and the Subarachnoid space
* Subdural space- between the arachnoid and dura mater, potential space
* Subarachnoid space- between the pia and arachnoid mater, where the cerebrospinal fluid and blood vessels are located
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The subarachnoid space structures
There are regions in the Subarachnoid space which are quite large which form cisterns. The subarachnoid space is divided by the trabeculae that join the arachnoid to the pia mater
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The Dura blood supply- main arteries
* Anterior meningeal artery
* Middle meningeal artery
* Accessory meningeal artery
* Posterior meningeal artery
* ,Other meningeal branches
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Location of the arteries in the dura mater
The blood supply travels in the outer periosteal layer, the main contribution is from the middle meningeal artery which is a branch of the maxillary artery from the external carotid. It divides into frontal and parietal branches within the skull. The accessory meningeal artery is a branch of the middle meningeal artery.
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Why is the middle meningeal artery so susceptible to injury
It lies beneath the pterion which is the thinnest part of the skull. Fractures in the pterion result in sharp bone fragments piercing the middle meningeal artery causing an extradural haematoma
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The Dural innervation- divisions of the trigeminal nerve CNV
* Ophthalmic CNV1- main branch
* Maxillary CNV2
* Mandibular CNV3
* Other contributions from the first three cervical nerves
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Dural venous sinuses
These sinuses are formed between the two layers of the dura mater. They receive blood from the superficial and deep cerebral veins. There are no valves so venous blood can flow in both directions, direction of flow depends on the local venous pressure at the time. They are drained by the internal jugular vein.
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Types of dural venous sinuses
1) Superior sagittal sinus
2) Confluence of sinuses
3) Right transverse sinus
4) Inferior sagittal sinus
5) Straight sinus
6) Left/right transverse sinus
7) Sigmoid sinus
8) Superior/inferior petrosal sinus
9) Cavernous sinus
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Superior sagittal sinus
Runs along the superior aspect of the falx cerebri, ends at the confluence of sinuses
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Right transverse sinus
Continuation of the confluence of sinuses
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Inferior sagittal sinus continuation
Runs along the inferior margin of the falx cerebri, joins to form the straight sinus. The straight sinus runs in the junction of the falx cerebri and the Tenorium cerebelli. The left transverse sinus is a continuation of the straight sinus.
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Sigmoid sinus
Continuation of the transverse sinus, they receive blood from the superior petrosal sinus. The superior petrosal sinus unites with the inferior petrosal sinus to form the internal jugular vein which exists the jugular foramen
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Cavernous sinus
Paired veins which are connected by the intercavernous sinus’s. The Cavernous sinus’s can drain into the Transverse sinus via the Superior petrosal sinus. Or drainage via the Inferior petrosal sinus into the internal jugular vein. The Cavernous sinuses are really important, they are a bilateral plexus of veins. They have connections to the orbit via the ophthalmic vein, face and the cerebral hemisphere via the cerebral vein
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The structures which pass through the Cavernous sinuses
```
O TOM CAT
• Oculomotor CN3
• Trochlear CN4
• Ophthalmic division- trigeminal CN5
• Maxillary division- trigeminal CN5
• Carotid artery (internal abducent CN6)
• Abducent nerve CN6
• T represents the levels of the carotid and abducent i.e. in line with the trochlear nerve
```
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Cavernous sinus pathology
Because there are many connections from the cavernous sinus to the face, orbit and nose any infection within these regions can cause intercranial spread. Can cause meningitis, abscess formation or a subdural empyema where there is pus between the dura and the arachnoid mater. Infection can also lead to thrombus formation within the cavernous sinus which can compress structures which can cause a cranial nerve palsy or a stroke if it compresses the internal carotid artery.
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Ventricular system
Cavities within the brain. Responsible for the production, transport and removal of cerebrospinal fluid
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Structure of lateral ventricle
Largest ventricle, has a body, anterior horn, atrium, a posterior horn and an inferior horn. The lateral ventricle goes through the interventricular foramen to the third ventricle. It then passes through the cerebral aqueduct to the 4th ventricle. Paired structure within the cerebral hemisphere, body of the lateral ventricle is within the parietal lobe. The anterior horn projects into the frontal lobe, the posterior horn projects into the occipital lobe and the inferior horn projects into the temporal lobe.
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Relations of the lateral ventricle
Above the lateral ventricle is the corpus callosum which connects both cerebral hemisphere. Below the lateral ventricle is the Thalamus and deep brain nuclei. The body and the anterior horn of the lateral ventricle is divided by the Septum pellucidum (membrane).
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Relations of the third ventricle
Thin structure, the lateral wall is made of the thalamus. The Hypothalamus is also near the third ventricle
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Relations of the fourth ventricle
Posteriorly they have the Cerebellum, anteriorly you have the pons and the medulla. The most causal point of the cerebellum is the ovex
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Where is the choroid plexus found
In the lateral, 3rd and 4th ventricle
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Enlargments of the sub-arachnoid space (cisterns)
* Cerebello-medullary cistern= made up of the posterior and lateral cerebello-medullary cistern.
* Pontocerebellar cistern- within the pons of the brainstem
* Interpeduncular cistern
* Chiasmatic cistern- near the optic chiasm
* Quadrigeminal cistern
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CSF reabsorption
Through the arachnoid granulations. These are projections of the arachnoid mater into the dural sinus's that allow the CSF to pass from the subarachnoid space to the venous system. CSF get reabsorbed because the hydrostatic pressure within the subarachnoid space is higher then in the lumen of the sinus
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Hydrocephalus
There are two types:
• Communicating- overproduction of CSF (rare) or blockage in reabsorption
• Non-communicating- the flow of CSF is impaired
Hydrocephalus caused widening of the ventricles and puts pressure on the tissues in the brain. Causes a headache, blurred or double vision and confusion
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Structures which are prone to narrowing within the ventricular system
Interventricular foramen, cerebral aqueduct, the lateral and median foramin
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What structures is the 4th ventricle related to
Pons, medulla and cerebellum
