NE Exam 1 Clinical Flashcards
Complete Lectures for CNs:
Triangles of Neck Dural Sinus Scalp/Superficial Face Skull Deep Face, TMJ Pterygopalatine Fossa/Nasal Cavity Oral Cavity & Pharynges Anatomy & Histology of the Ear Brauer
Embryo Lectures’ CNs in Summary Sheets
Remaining:
Cranial Nerves
Orbit, Eye, & Eye Movements Stephens
Retropharyngeal Space
Easy route for upper respiratory or oral infections to spread. Allows movement, infection goes from occipital bone down to esophagus.
(Text Ref)
Pus from an abscess posterior to the prevertebral layer of deep cervical fascia may extend laterally in the neck and form a swelling posterior to the SCM. The pus may perforate the prevertebral layer of deep cervical fascia and enter the retropharyngeal space, producing a bulge in the pharynx (retropharyngeal abscess). This abscess may cause difficulty in swallowing (dysphagia) and speaking (dysarthria).
Infections in the head may also spread inferiorly posterior to the esophagus and enter the posterior mediastinum, or it may spread anterior to the trachea and enter the anterior mediastinum. Infections in the retropharyngeal space may also extend inferiorly into the superior mediastinum. Similarly, air from a ruptured trachea, bronchus, or esophagus (pneumomediastinum) can pass superiorly in the neck.
Nerve Point of Neck
Site of application of anesthetic (mid-SCM)
(Text Ref)
For regional anesthesia before neck surgery, a cervical plexus block inhibits nerve impulse conduction. The anesthetic agent is injected at several points along the posterior border of the SCM, mainly at the junction of its superior and middle thirds, the nerve point of the neck (Figs. 9.9 and 9.14A). Half of the diaphragm is usually paralyzed by a cervical plexus block, due to the inclusion of the phrenic nerve in the block. Therefore, this procedure is not performed on persons with pulmonary or cardiac disease.
Torticollis
Pathology of SCM causing head to turn to side and the face to turn away from affected side.
• Congenital torticollis– fibrous tissue tumor within SCM that develops in utero. Causes head to turn to side and the face to turn away from affected side– shortens SCM.
• Muscular torticollis– occasionally SCM may be injured during difficult birth, tearing its fibers leading to hematoma that develops into fibrotic mass the entraps part of CN 11 effectively denervating it. Stiffness of neck then results from fibrosis and shortening of SCM. May require surgical detaching of SCM.
Tx: PT or Surgery
(Text Ref)
Congenital Torticollis: Torticollis (L. tortus, twisted + L. collum, neck) is a contraction or shortening of the cervical muscles that produces twisting of the neck and slanting of the head. The most common type of torticollis (wry neck) results from a fibrous tissue tumor (L. fibromatosis colli) that develops in the SCM before or shortly after birth. The lesion, like a normal unilateral SCM contraction, causes the head to tilt toward, and the face to turn away from, the affected side (Fig. B9.1). When torticollis occurs prenatally, the abnormal position of the infant’s head usually necessitates a breech delivery.
Occasionally, the SCM is injured when an infant’s head is pulled too much during a difficult birth, tearing its fibers (muscular torticollis) (Kliegman et al., 2016). A hematoma (localized mass of extravasated blood) occurs that may develop into a fibrotic mass that entraps a branch of the spinal accessory nerve (CN XI) and thus denervates part of the SCM. The stiffness and twisting of the neck results from fibrosis and shortening of the SCM. Surgical release of the SCM from its inferior attachments to the manubrium and clavicle inferior to the level of CN XI may be necessary to enable the person to hold and rotate the head normally
Spasmodic Torticollis: Cervical dystonia (abnormal tonicity of the cervical muscles), commonly known as spasmodic torticollis, usually begins in adulthood. It may involve any bilateral combination of lateral neck muscles, especially the SCM and trapezius. Characteristics of this disorder are sustained turning, tilting, flexing, or extending of the neck. Shifting the head laterally or anteriorly can occur involuntarily (Fahn, 2016). The shoulder is usually elevated and displaced anteriorly on the side to which the chin turns
Severance of Phrenic Nerve (C3-5), Phrenic Nerve Block, and Phrenic Nerve Crush
Severance of phrenic or phrenic nerve block– paralysis of that side of diaphragm
(Text Ref)
Severance of a phrenic nerve results in paralysis of the corresponding half of the diaphragm. A phrenic nerve block produces a short period of paralysis of the diaphragm on one side (e.g., for a lung operation). The anesthetic is injected around the nerve where it lies on the anterior surface of the middle third of the anterior scalene muscle. A surgical phrenic nerve crush (e.g., compressing the nerve injuriously with forceps) produces a longer period of paralysis (sometimes for weeks after surgical repair of a diaphragmatic hernia). If an accessory phrenic nerve is present, it must also be crushed to produce complete paralysis of the hemidiaphragm.
Where will bleeding be controlled by the compression of Subclavian Artery against the rib?
Upper Limb
Dysphonia
Hoarseness
Laryngitis
Dysphonia– disorder of the voice
Hoarseness–inflammation of vocal cords
Laryngitis–inflammation of vocal cords where no longer vibrate
Injury to Recurrent Laryngeal Nerves
Damage to left recurrent laryngeal causes loss of vocalization
(Test Ref)
The risk of injury to the recurrent laryngeal nerves is ever present during neck surgery. Near the inferior pole of the thyroid gland, the right recurrent laryngeal nerve is intimately related to the inferior thyroid artery and its branches (Fig. B9.10). This nerve may cross anterior or posterior to branches of the artery, or it may pass between them. Because of this close relationship, the inferior thyroid artery is ligated some distance lateral to the thyroid gland, where it is not close to the nerve. Although the danger of injuring the left recurrent laryngeal nerve during surgery is not as great, owing to its more vertical ascent from the superior mediastinum, the artery and nerve are also closely associated near the inferior pole of the thyroid gland (Fig. 9.28). Hoarseness is the usual sign of unilateral recurrent nerve injury; however, temporary aphonia or disturbance of phonation (voice production) and laryngeal spasm may occur. These signs usually result from bruising the recurrent laryngeal nerves during surgery or from the pressure of accumulated blood and serous exudate after the operation.
Occlusion of Cerebral Veins & Dural Venous Sinuses
Danger triangle, ophthalmic vein can bring the infection there.
(Text Ref)
Occlusion of cerebral veins and dural venous sinuses may result from thrombi (clots), thrombophlebitis (venous inflammation), or tumors (e.g., meningiomas). The dural venous sinuses most frequently thrombosed are the transverse, cavernous, and superior sagittal sinuses.
The facial veins make clinically important connections with the cavernous sinus through the superior ophthalmic veins. Cavernous sinus thrombosis usually results from infections in the orbit, nasal sinuses, and superior part of the face (the danger triangle, Fig. B8.17). In persons with thrombophlebitis of the facial vein, pieces of an infected thrombus may extend into the cavernous sinus, producing thrombophlebitis of the cavernous sinus. The infection usually involves only one sinus initially, but it may spread to the opposite side through the intercavernous sinuses. Thrombophlebitis of the cavernous sinus may affect the abducent nerve as it traverses the sinus and may also effect the nerves embedded within the lateral wall of the sinus. Septic thrombosis of the cavernous sinus often results in the development of acute meningitis.
Thrombophlebitis of Facial Vein
The facial vein makes clinically important connections with the cavernous sinus through the superior ophthalmic vein, and the pterygoid venous plexus through the inferior ophthalmic and deep facial veins (Figs. 8.25 and 8.29A; Table 8.6). Because of these connections, an infection of the face may spread to the cavernous sinus and pterygoid venous plexus.
Blood from the medial angle of the eye, nose, and lips usually drains inferiorly through the facial vein, especially when a person is erect. Because the facial vein has no valves, blood may pass through it in the opposite direction. Consequently, venous blood from the face may enter the cavernous sinus. In individuals with thrombophlebitis of the facial vein—inflammation of the facial vein with secondary thrombus (clot) formation—pieces of an infected clot may extend into the intracranial venous system and produce thrombophlebitis of the cavernous sinus. Infection of the facial veins spreading to the dural venous sinuses may result from lacerations of the nose or be initiated by squeezing pustules (pimples) on the side of the nose and upper lip. Consequently, the triangular area from the upper lip to the bridge of the nose is considered the danger triangle of the face (Fig. B8.17).
Cavernous Sinus Thrombosis
Clinical: High fever, periorbital edema (swelling around eyes) and chemosis (irritation of eyes), CN VI palsy (lateral gaze), & decreased visual acuity.
Abducens N. (VI) can also be affected by thrombosis there.
Dx: CT scan & MRi
Rx: IV ABX, Heparin, Surgery
Hydrocephalus
- “water on the brain’
- typically from an obstruction in csf flow that restricts its reabsorption in the venous bloodstream
- treated by inserting a ventriculoperitoneal shunt that drains to the abdominal cavity…
- or a ventriculostomy (ETV) that creates a hole in the floor of the third ventricle that drains into the subarachnoid space
(Text Ref)
Overproduction of CSF, obstruction of CSF flow, or interference with CSF absorption results in excess fluid in the cerebral ventricles and enlargement of the head, a condition called obstructive hydrocephalus (Fig. B8.20A). The excess CSF dilates the ventricles, thins the cerebral cortex, and separates the bones of the calvaria in infants. Although an obstruction can occur any place, the blockage usually occurs in the cerebral aqueduct (Fig. B8.20B) or an interventricular foramen. Aqueductal stenosis (narrow aqueduct) may be caused by a nearby tumor in the midbrain or by cellular debris following intraventricular hemorrhage or bacterial and fungal infections of the central nervous system.
Blockage of CSF circulation results in dilation of the ventricles superior to the point of obstruction and increased pressure on the cerebral hemispheres. This condition squeezes the brain between the ventricular fluid and the calvarial bones. In infants, the internal pressure results in expansion of the brain and calvaria because the sutures and fontanelles are still open. It is possible to produce an artificial drainage system to bypass the blockage and allow CSF to escape, thereby lessening damage to the brain.
In communicating hydrocephalus, the flow of CSF through the ventricles and into the subarachnoid space is not impaired. However, movement of CSF from this space into the venous system is partly or completely blocked. The blockage may be caused by the congenital absence of arachnoid granulations, or the granulations may be blocked by red blood cells as the result of a subarachnoid hemorrhage.
Epidural Hematoma
Blow to temporal region (fracture) can rupture the middle meningeal A. leading to epidural hematoma (between Dura Mater and Bone).
(Text Ref)
Extradural (epidural) hemorrhage is arterial in origin. Blood from torn branches of a middle meningeal artery collects between the external periosteal layer of the dura and the calvaria. The extravasated blood strips the dura from the cranium. Usually this follows a hard blow to the head, and forms an extradural (epidural) hematoma. Typically, a brief concussion (loss of consciousness) occurs, followed by a lucid interval of some hours. Later, drowsiness and coma (profound unconsciousness) occur. Compression of the brain occurs as the blood mass increases, necessitating evacuation of the blood and occlusion of the bleeding vessel(s)
Vertebrobasilar Insufficiency
- decreased posterior circulation due to intermittent vertebral artery occlusion:
- from atherosclerosis
- during head rotation or extension
- symptoms:
- syncope, vertigo, dizziness
- double vision or loss of vision
- numbness or weakness in hands or feet
- slurred speech
- nausea & vomiting
- loss of coordination or weakness
- risk factors include:
- smoking
- hypertension or hyperlipidemia
- diabetes or obesity
- over 50 years old
- family history
- diagnosed:
- history & physical
- cardiovascular and neurologic exams
- ct angiogram/mra looking at blood vessels
- treatment
- change diet
- quit smoking
- lose weight/become more active
- medications to control bp, diabetes, cholesterol
- medications to thin blood or reduce coagulation
- bypass surgery or endarterectomy
Subclavian Steal Syndrome
- proximal stenosis or occlusion of the subclavian artery
- blockage causes reverse flow through the vertebral artery of the affected side to supply blood to upper extremity
- decreasing blood flow to the brain
- symptoms:
- presyncope or syncope
- different blood pressures in the upper extremities
- neurologic deficits or memory problems
- causes:
- atherosclerosis
- cervical rib
- diagnosis:
- doppler ultrasound
- CT angiography
- treatment:
- stent & balloon angioplasty
- endarterectomy
Scalp Injury: Superficial Injury
superficial to aponeurosis
• Does not gap as aponeurosis holds edges of wound together
Scalp Injury: Deep Injury
through aponeurosis
• Forms gaping wound because of pull of occipitofrontalis muscle
Why do scalp injuries bleed profusely?
How do scalp infections spread into cranium?
CT of scalp tends to hold cut vessels open
via small emissary veins (anastomoses between intra- and extracranial veins)
SCALP
Skin, Dense CT, Aponeurosis, Loose Ct (site for infection), Periosteum
Bell’s Palsy
Facial nerve injury: damage due to surgery or infections causes Bell’s palsy; muscle weakness/paralysis including inability to close eyelids– prone to cornea ulceration
If you cant blink you cant rejuvenate tears over cornea (a vascular, needs tears for nutrients, O2, etc), so can cause tear in cornea
Botox Injections
Innervation of Facial Expression Muscle CN VII
Botox injections (Botulinum toxin)–blocks neuromuscular transmission by inhibiting acetylcholine release; used to treat eye disorders, migraines, muscle spasms or used cosmetically
Nerve will eventually recover and will need to inject again
Herpes Zoster Virus
• Chickenpox virus—initial infection
• Lesions due to reactivation of virus that can appear anywhere on the body
• Many produce lesions in cranial ganglia with most involving CN V (75%)
• Ophthalmic division commonly affected (25%)
• Usual cornea involved accompanied by leading to painful corneal ulceration
Lesions outlining region innervated by V1.
Virus inactive stays in nerve cells, can resurge and reactivate. Go to nerve endings and cause lesions.
Shingles vaccine can reduce risk of resurgence.
An exterior infection can travel into vascular and then into the cranial vault via an anastomoses between what veins?
Supratrochlear, supraorbital, angular vein of facial vein with intracranial veins
Surgical Access to Cranial Cavity: Bone Flaps
- The periosteum has poor osteogenic properties.
- Bone wired or plated while healing.
- Healing best when flap incorporates overlaying tissues (e.g. skin, muscle, fascia)
Periosteum doesn’t fuse back well
Best healing when overlaying tissues
What are the three types of Le Fort fractures?
Le Fort I is a fracture of the maxilla localized to the alveolar process of the maxilla.
Le Fort II is partially through the orbit, and damages the maxilla up to the zygomatic maxillary suture.
Le Fort III is a detachment of the upper portion of the face from the cranium.
Cleft Lip vs Cleft Palate
(Not sure if my notes are accurate for this)
Lack of fusion
Cleft Palate: Posterior fusion of Palatine bone and part of the Maxilla
Cleft Lip: Run all, comes forward, tongue can slip into nose, more of maxilla
(Text Ref) Cleft lip (harelip, a misnomer) is a birth defect (usually of the upper lip) that occurs in 1 of 1,000 births; 60–80% of affected infants are males. The clefts vary from a small notch in the transitional zone of the lip and vermilion border to a notch that extends through the lip into the nose. In severe cases, the cleft extends deeper and is continuous with a cleft in the palate. Cleft lip may be unilateral or bilateral.
Cleft palate, with or without cleft lip, occurs in approximately 1 of 2,500 births and is more common in females than in males. The cleft may involve only the uvula, giving it a fishtail appearance, or it may extend through the soft and hard regions of the palate. In severe cases associated with cleft lip, the cleft palate extends through the alveolar processes of the maxillae and the lips on both sides. The embryological basis of cleft palate is failure of mesenchymal masses in the lateral palatine processes to meet and fuse with each other, with the nasal septum, and/or with the posterior margin of the median palatine process.
Dislocation of TMJ
(Text Ref)
Sometimes during yawning or taking a large bite, excessive contraction of the lateral pterygoids may cause the heads of the mandible to dislocate anteriorly (pass anterior to the articular tubercles). In this position, the mandible remains depressed and the person is unable to close his or her mouth. Most common, a sideways blow to the chin by a clenched hand (fist) when the mouth is open dislocates the TMJ on the side that received the blow. Dislocation of the TMJ may also accompany fractures of the mandible. Posterior dislocation is uncommon, being resisted by the presence of the postglenoid tubercle and the strong intrinsic lateral ligament. Usually in falls on or direct blows to the chin, the neck of the mandible fractures before dislocation occurs. Because of the close relationship of the facial and auriculotemporal nerves to the TMJ, care must be taken during surgical procedures to preserve both the branches of the facial nerve overlying it and the articular branches of the auriculotemporal nerve that enter the posterior part of the joint. Injury to articular branches of the auriculotemporal nerve supplying the TMJ, associated with traumatic dislocation and rupture of the articular capsule and lateral ligament, leads to laxity and instability of the TMJ.
Inferior Alveolar N. Block
Not sure if this was a CN from Deep Face, TMJ Lecture.
Numb whole mouth by injecting anesthetic to Inferior Alveolar N.
(Text Ref)
An inferior alveolar nerve block anesthetizes the inferior alveolar nerve, a branch of CN V3. The site of the anesthetic injection is around the mandibular foramen, the opening into the mandibular canal on the medial aspect of the ramus of the mandible (Fig. 8.75). This canal gives passage to the inferior alveolar nerve, artery, and vein. When this nerve block is successful, all mandibular teeth are anesthetized to the median plane. The skin and mucous membrane of the lower lip, the labial alveolar mucosa and gingivae, and the skin of the chin are also anesthetized because they are supplied by the mental nerve, a branch of the inferior alveolar nerve. There are possible problems associated with an inferior alveolar nerve block, such as injection of the anesthetic into the parotid gland or the medial pterygoid muscle. This would affect ability to open the mouth (pterygoid trismus).
Infraorbital Nerve Block
Not sure if this was a CN from Deep Face, TMJ Lecture.
(Text Ref)
For treating wounds of the upper lip and cheek or, more commonly, for repairing the maxillary incisor teeth, local anesthesia of the inferior part of the face is achieved by infiltration of the infra-orbital nerve with an anesthetic agent. The injection is made in the region of the infra-orbital foramen, by elevating the upper lip and passing the needle through the junction of the oral mucosa and gingiva at the superior aspect of the oral vestibule.
To determine where the infra-orbital nerve emerges, pressure is exerted on the maxilla in the region of the infra-orbital foramen. Too much pressure on the nerve causes considerable pain. Because companion infra-orbital vessels leave the infra-orbital foramen with the nerve, aspiration of the syringe during injection prevents inadvertent injection of anesthetic fluid into a blood vessel. Because the orbit is located just superior to the injection site, a careless injection could result in passage of anesthetic fluid into the orbit, causing temporary paralysis of the extra-ocular muscle.
