Subaxial Cervical Spine Injuries: Introduction

• Common cause of disability 
• Most common causes:–  RTA, Fall, Penetrating trauma, Sports 
• Highly prone to traumatic injury:
• Mobile, relatively unprotected, and its high position 
• 60% of all spinal injuries occur in the cervical spine 
• Subaxial cervical spine injuries include:
• 2/3rd of all cervical fractures
• 75% of all cervical dislocations 
• One third of injuries occur at the level of C2, and one half of injuries occur at the level of C6 or C7.

Subaxial Cervical Spine Injuries: Epidemiology

• Bimodal Peak
• Adolescents and Young Adults
• Middle Aged Individuals (55 years)
• Males accounts for 80% of injuries 

3/11/2021 08:32:00 AM

Contents

1. Case Report
2. Introduction
3. Signs and symptoms
4. Pathophysiology
5. Diagnosis
6. Treatment
7. Hypertensive Pontine Hemorrhage Video

Case Report

• 52yr old male
• k/c/o HTN not on regular medication
• Presented with sudden onset loss of consciousness

On Examination

• GCS - E1VetM1
• Pupils -B/L 1mm NRTL (Pin-Point Pupils)
• Planters B/L mute

CT Scan

Hypertensive Pontine Hemorrhage

Hypertensive Pontine Hemorrhage: Introduction

• Seen in long standing poorly-controlled chronic hypertension. 
• It carries a very poor prognosis.
• Pontine hemorrhage accounts for 5-10% of all hemorrhagic strokes (Jang et al 2011)

Signs and symptoms

• "classic" pontine hematoma syndrome characterized by coma, quadriparesis, and eventual demise (Kushner et al 1985)
• Clinical features of Pontine Hematoma are (Deng and Gaillard et al.)
• • Loss of consciousness (most common)
  • long tract signs including tetraparesis
  • cranial nerve palsies
  • seizures
  • Cheyne-Stokes respiration
• CST does not play an essential role in recovery of independent walking and vestibulospinal tracts may not crucially affect recovery of independent walking in patients with pontine hemorrhage. In contrast, and intact CRP (corticoreticular pathway) or changes of the CRP integrity appear to be related to the recovery of gait function (Yeo et al 2020)

Pathophysiology

Hypertensive Pontine Hemorrhage

• Due to rupture of penetrating arteries from the basilar artery extending into the pons 
• These arteries are prone to lipohyalinosis as a result of poorly-controlled hypertension 
• This makes the vessel wall prone to rupture. 
• Larger paramedian perforators are more commonly the culprit vessels

Other Causes of Pontine Hemorrhage

Other causes of pontine hemorrhage include

• Cavernoma
• AV Malformation
• Tumour bleed
• Transtentorial herniation (Duret Hemorrhage)

Diagnosis

NCCT Brain is the investigation of choice. It shows:

• Acute intraparenchymal hemorrhage within the pons
• The hematoma frequently ruptures into the 4th ventricle 

Treatment

• Poor prognosis
• Large bleeds are almost universally fatal. 
• Open surgical evacuation of the clot is usually not performed
• In smaller hemorrhages, medical management and treatment of hydrocephalus with extraventricular drains may be life saving, 
• Mortality ranges between 30% and 90% (Jang et al 2011)
• Outcome depends on the volume of the bleed and initial GCS

Hypertensive Pontine Hemorrhage Video

Hypertensive Pontine Hemorrhage Video

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1. Neurogenic bladder refers to dysfunction of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition . 

2. Non Neurogenic bladder refers to dysfunction of the urinary bladder due to dynamic disturbance of genitourinary system. 

 

Micturition Pathway

3. detrusor muscle of the bladder is innervated by parasympathetic neurons located in the S2-S4  column

 

5/19/2020 01:08:00 AM

 


1. MR spectroscopy provides a measure of brain chemistry.
2. The most common nuclei that are used are 
• 1H (proton)
• 23Na (sodium)
• 31P (phosphorus). 
• Proton spectroscopy is easier to perform and provides much higher signal-to-noise than either sodium or phosphorus.
3. MRS can be performed within 10-15 minutes and can be added on to conventional MR imaging protocols. 
4. It can be used to serially monitor biochemical changes in tumors, stroke, epilepsy, metabolic disorders, infections, and neurodegenerative diseases. 
5. They require interpretation and should always be correlated with the MR images before making a final diagnosis.

5/05/2020 01:23:00 AM

 Video Link:Neurosurgery written board crash course - hypothalamus 




 

1. hypothalamus as the name suggests is directly underneath the thalamus and it's directly above the pituitary 
2. borders of the hypothalamus can be drawn by a triangle 
• line between the anterior commissure and a posterior commissure and it's called the ACPC line
• line between the anterior commissure and the optic chiasm roughly boarded by the lamina terminalis 
• line between the chiasm and the posterior commissure 

5/02/2020 09:39:00 PM

What are the pain sensitive intracranial structures?

Brain itself is pain insensitive. 

The following intracranial structures are pain-sensitive:

1. Meningeal arteries
2. Proximal portions of the cerebral arteries
3. Dura at the base of the brain
4. Venous sinuses
5. Cranial nerves 5, 7, 9, and 10, and cervical nerves 1, 2, and 3

What are the mechanisms causing headaches?

• Distortion or traction of Dura, Venous Sinuses or Blood vessels: 

• Drainage of CSF in erect posture causes headache, secondary to traction on the venous sinuses when the brain sinks toward the tentorium as it loses CSF flotation
• Intracranial mass distorts the dura or the arteries at the base of the brain 
• Distortion due to raised ICP 

• Distension of a vessel

• Distension of extracranial and occasionally intracranial arteries is thought to be the cause of pain in migraine (activate the trigeminal nerve terminals in the vessel wall)

• Inflammation

• Inflammation in the subarachnoid space can result in headache. Inflammation can be caused by infection, hemorrhage, or chemical irritation
• Inflammation of vessel wall by autoimmune process. eg Giant cell arteritis

• Referral of Pain

• Lesions above the tentorium - referred pain in trigeminal nerve distribution (the forehead or behind the eye) - because the dura in this region is supplied by the trigeminal nerve
• Lesions in the posterior fossa - 
• referred pain in the ear and the back of the head - because this part of the dura is supplied by cranial nerves 9 and 10 and the upper three cervical roots
• refer pain to orbit -  termination of orbital (ophthalmic division) pain nerve fibers in the lowest part of the spinal nucleus of the trigeminal nerve, which also receive termination of the upper cervical pain afferent nerve fibers 
• referred pain to ear - Irritation of cranial nerves 7, 9, and 10 - because the ear has cutaneous supply from each of these nerves as well as cranial nerve 5.

What are the types of Headaches?

For the purpose of history taking, headaches can be divided into two types:

• Primary- no identifiable cause on examination or investigation and diagnosis is based on  recognizing a pattern, e.g.
• Migraine
• Cluster headache
• Tension-type headache
• Secondary - definite identifiable cause on examination or investigation, e.g. 
• Brain tumors
• Meningitis
• Sub-arachnoid hemorrhage 
• 90% - primary headaches, less than 10% are secondary headaches (Rasmussen 1991)

What are the headache "Red Flags"?

• Worst Headache ever
• New onset Headache
• Onset after age of 50 yrs
• Change in pattern of headache
• Worsening headache
• Sudden onset during exertion, sneezing, coughing
• Headache with postural variation
• Headache in setting of malignancy or HIV
• Headache associated with Neurological symptoms or signs
• Associated with systemic symptoms - fever, weight loss and chronic cough

What history to take in a patient presenting with Headache?

Duration

Exact duration as reported by patient

NEW onset headache or something that has been there since before and has worsened now

Onset ( sudden/ gradual )

Acute onset, severe, first and worst headache, the common possibilities are sub-arachnoid hemorrhage, vascular dissection, pituitary apoplexy

Gradual onset – migraine(mins to days), SDH, GCA(days to months)

Severity

verbal rating scale from 0 to 10

Character

Pulsatile or throbbing or hammering (Raised ICP Headaches/ Migraine)

Dull featureless pain (Tension type headache)

Boring sharp- cluster HA

Time of occurrence

Raised ICP headaches - More in morning, May waken the patient at an early hour

Frequency

Increase in frequency - red flag

Distribution

Frontal or Holocranial - Raised ICP

Band like - tension headaache

Aggravating factors

Exertion, coughing, sneezing, stooping, and straining at stool

Changes in posture (increases in supine - ↑ICP , increases in upright – low CSF pressure headache)

Relieving factors

Improvement on lying flat - low pressure headache

Associated features

Blurring of Vision - Papilloedema

Diplopia, the commonest cause of which is abducens nerve paresis

Nausea & vomiting – migraine, ↑ICP

Neck stiffness – meningeal process

Changes in consciousness

Focal neurological symptoms

References

• Ravishankar K. The art of history-taking in a headache patient. Ann Indian Acad Neurol. 2012;15(Suppl 1):S7–S14. doi:10.4103/0972-2327.99989
• Rasmussen BK, Jensen R, Schroll M, Olesen J. Epidemiology of headache in a general population – a prevalence study. J Clin Epidemiol. 1991;44:1147–57
• https://www.dartmouth.edu/~dons/part_2/chapter_18.html

12/24/2019 10:06:00 PM