1
2	Anatomy of a Long Bone
3	Bone Development Enchondral ossification cartilage model of much of the skeleton is formed from the mesenchyme extremities, spine, base of the skull Intramembranous ossification bone tissue replaces membranous fibrous skull
4	Primary Ossification Centers Present before birth one for centrum two for each neural arch
5	Secondary Ossification Centers Present after birth epiphysis forms articular cartilage gives length to bone apophysis attachment for ligament & tendons
6	Block Segmentation (p. 333)
7	Clinical Data failure of somite segmentation most common at C5/C6, C2/C3, L4/L5 aka “fusion” nonsegmentation Significance minimal clinical significance or risk may create aberrant segmental motion above and below the fusion site DDx surgical fusion pathological fusion juvenile chronic arthritis infection
8	Imaging rudimentary disc sometimes with calcification maintenance of vertebral body height smooth, often concave anterior vertebral body margins Wasp vertebra well formed foramen on the lateral projection Additional Studies flexion/extension x-rays to evaluate adjacent segmental motion
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10
11	Surgical vs. Congenital
12	Failure of Fusion of C1 Neural Arch (p. 333) Spina bifida occulta, dysraphism, or rachischisis
13	Clinical Data defective ossification of the cartilage anlage composed of cartilage and fibrous tissue Significance no clinical significance or risk DDx none! fracture too smooth no relevant trauma
14	Imaging cleft or complete absence absence of spinolaminar line on lateral hyperplastic anterior arch
15	Imaging failure of fusion anterior arch of C1
16	Agenesis Posterior Arch
17	Occipitalization (assimilation) of the Atlas
18	Clinical Data Typically, the anterior arch of the atlas is fused to the skull base one half of patients with occipitalization of the atlas also have vertebral fusion at the C2-C3 spinal level although the odontoid process is high, directly beneath the foramen magnum basilar impression is uncommon Significance is a normal variant that is asymptomatic in most cases hypermobiliy at the ADI see craniovertebral anomalies discussion
19	Imaging evidence of fusion Additional Studies flexion and extension sometimes needed to assure diagnosis Also ADI CT with reformatting on rare occasion
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22	Occipitalization Can have partial or complete congenital fusion of the atlas to the occiput Occipitalization can lead to symptomatic chronic atlanto-axial instability and cord impingement Symptoms include weakness, atrophy, spasticity, headache, which are usually slow onset, but sudden death has been associated with the condition (traumatic in ½, major or minor) If the dens is in the foramen magnum, crowding of anterior elements can result. Usually asymptomatic if dens lies below the foramen magnum. 60% have odontoid > 3mm displaced behind anterior arch of atlas. Constricting dural bands are commonly associated. Physical exam findings include short neck, low hairline, torticollis, restricted neck motion. 20% have other associated congenital anomalies.
23	Craniovertebral Anomalies basilar impression/occipitalization Chiari malformation renal anomalies potential neurological compromise posterior column signs long tract signs consider MRI
24	Chiari Malformation (p. 1395) herniation of the cerbellar tonsils ectopia less than 3mm = normal varint Significance associated with “wrong way” scoliosis bony anomalies Syrinx/syringomyelia Imaging MRI
25	Pathophysiologic Mechanisms underdevelopment of the occipital somites produces a diminutive, overcrowded posterior cranial fossa. Tonsillar herniation occurs secondarily as a result of mechanical factors. Altered CSF dynamics which is characterized by systolic and diastolic CSF displacements related to the phases of the cardiac cycle. Respiration also affects CSF flow pulsation. As the herniated tonsils fill the foramen magnum in the setting of CMI, CSF flow is reduced at the craniovertebral junction, and a compensatory pulsatile descent of the cerebellar tonsils is observed during systole. This combination can effectively plug the CSF pathway at the foramen magnum.
26	“wrong way” scoliosis left convex scoliosis thoracic spine Significance syringomyelia Arnold Chiari malformation neurology examination Imaging do MRI with neurological symptoms and adults do MRI in all children
27	Syringomyelia spinal cord cavity (syrinx) Etiology pressure tumor congenital Arnold Chiari secondary to pathologic CSF dynamics. The exaggerated pulsatile systolic wave in the spinal subarachnoid space drives the CSF through anatomically continuous perivascular and interstitial spaces into the central canal of the spinal cord. Imaging MRI
28	Associated Osseous Anomalies Platybasia, basilar invagination (25-50%) Atlantooccipital assimilation (1-5%) Klippel-Feil syndrome (5-10%) Incomplete ossification of C1 ring (5%) Proatlantal remnant spina bifida at the C1 level Retroflexed odontoid process (26%) Scoliosis (42%) Kyphosis Increased cervical lordosis Cervical ribs Fused thoracic ribs
29	Side Note Always KNOW the diagnosis in ALL patients with neurological signs – BEFORE you adjust In other words know the anatomy Do NOT make subluxation a “garbage bucket” diagnosis These can all “look” the same subluxation Disc hernation multiple sclerosis syrinx cord tumor spinal stenosis IVF stenosis
30	Posterior Ponticle (p. 317) ponticulus posticus posticus ponticus Kimmerly anomaly forms the arcuate foramen
31	Clinical Data ossification of the oblique portion of the atlanto-occipital ligament between the posterior aspect of the lateral mass and the posterior arch contains the vertebral artery and the first cervical nerve 14% of anatomic specimens Significance minimal clinical significance or risk question of vertebral artery occlusion
32	Imaging seen as bony bar forms the arcuate foramen DDX do not confuse with the mastoid process!
33	Epitransverse Process (p. 317)
34	Clinical Data bony extension originating from the transverse process of C-1 to end at the skull base (vs paracondylar process goes the opposite way) Significance may create lateral head tilt may affect adjusting technique effective fusion of C1 to the occiput
35	Imaging difficult on conventional radiography accessory joint may be seen on occasion Additional Studies may require tomography on rare occasion
36	Os Odontoideum (p. 323)
37	Odontoid process anomalies (p. 323) B- os terminale C- os odontoideum D- odontoid agenesis
38	Os Odontoideum
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40	Clinical Data lack of fusion of the odontoid process with the body of C-2 previous fracture of the odontoid synchondrosis associated with: Down’s syndrome Klippel-Feil syndrome Significance renders the transverse atlantal ligament incompetent potential for significant neurological insult from trivial trauma. high velocity adjusting contraindicated consider neurosurgical consultation DDX fracture appropriate history? smooth cortices
41	Clinical Data neurological symptoms variable often limited to one transitory episode of diffuse paresis following trauma or progressive myelopathy with weakness and ataxia vertebral artery compression with cervical and brainstem ischemia gait ataxia, syncope, vertigo, and visual disturbances. Later, cerebellar and brainstem infarcts and seizures may occur. Sudden death is rare but can occur. Physical examination of patients with os odontoideum includes a complete neck examination. Evaluate for pain, range of motion (ROM), and associated anomalies. A careful neurologic examination must include assessment of cerebellar and brainstem function. Gait evaluation and Romberg tests are helpful in diagnosing os odontoideum. Other upper motor neuron findings commonly are reported, including spasticity, hyperreflexia, clonus, and proprioceptive loss.
42	Clinical Data Indications for surgery include the following: Significant motion on plain radiography Neurologic or neurovascular involvement Persistent and disabling pain despite appropriate nonoperative management Suggestions for management are based on reports of small series and tend to vary between authors. Some authors report resolution of symptoms following transient paresis and recommend continued nonoperative management. Others operatively stabilize any patient reporting neurologic symptoms.
43	Imaging well corticated separate ossicle ossicle may be absent or difficult to see C1 subluxation short odontoid hypertrophic C1 anterior arch Additional Studies flexion/extension: evaluate instability MRI: evaluate cord compression/contusion
44	Os odontoideum with attenuation of the spinal cord necessitating surgical fusion
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46	Os odontoideum
47	Os Terminale (p. 323) Failure of union of the secondary center of ossification found at the tip of the dens. Usually seen after the age of 12 years old not associated with instability.
48	Klippel Feil Syndrome (p. 441)
49	Clinical Data complex of congenital anomalies that includes multiple segmentation anomalies of the cervical spine short webbed neck (pterygium colli) low hairline decreased range of motion associated with renal anomalies - 50% deafness (30%) spinal cord anomalies – syringomyelia and Arnold Chiari Sprengel’s deformity 25-40%
50	Imaging Initial studies include anteroposterior, AP open mouth and lateral views of the cervical spine. fusion of vertebral bodies and posterior elements hemivertebrae scoliosis rib fusion Sprengel deformity If anomalies are found, carefully assess the craniocervical junction to detect anomalies at that level. Flexion-extension radiographs are indicated if instability is suspected at the craniocervical junction Obtain plain radiographs of the entire spine to detect other spinal anomalies. Examine the chest to rule out involvement of the heart. Examine the chest wall for the possibility of rib anomalies, which can include multiple rib fusions. Rib fusions can be revealed with plain radiography.
51	Imaging Additional Studies flexion/extension ultrasound to demonstrate the presence of 2 functioning kidneys intravenous urogram neurological evaluation MRI
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53	Sprengels Deformity (p. 440)
54	Clinical Data Congenital elevation of scapula. incomplete descent of the scapula Seen in 20-25% of cases of Klippel Feil relatively rare in chiropractic practice
55	Klippel-Feil syndrome
56	Down syndrome Background: trisomy 21 Imaging: 20% of patient demonstrate laxity of the transverse atlantal ligament short posterior arch Clinical: Fattened nose, wide spaced eyes Mental retardation
57	Cervical Ribs
58	Clinical Data extra rib that articulates with the transverse process principally at C7, rarely C5 and C6 2: 1 females .5% of the population Significance thoracic outlet syndrome with neurovascular compression even with small ribs symptoms become more common in older population evaluate for peripheral vascular and neurological compromise DDX differentiate from an enlarged C7 transverse process-observed the articulation can be palpated and confused with an enlarged lymph node
59	Imaging evidence of bone articulating with the C7 transverse process downward deflecting transverse process = C7 Additional Studies thoracic outlet syndrome clinical examinations neurovascular studies EMG and doppler ultrasound on rare occasion
60	Transverse Process Hyperplasia Transverse process at C7 longer than T1
61	Butterfly Vertebra (p. 328)
62	Clinical Data failure of fusion of lateral halves secondary to persistence of notochordal tissue widened vertebral body with butterfly configuration (AP view) adaptation of vertebral endplates of adjacent vertebral bodies most common in the thoracic and lumbar spine Significance usually insignificant aberrant segmental motion probable
63	Imaging pronounced indentation of the endplate’s widening of the distance between the pedicles disk hypoplasia adjacently or possible fusion
64	Hemivertebra (p. 328)
65	Clinical Data vertebral body normally develops from two lateral ossification centers with a failure of growth occurring to form the hemivertebra lateral hemivertebra most common structural scoliosis Significance scoliosis aberrant segmental motion inclusive of fusion associated with other congenital anomalies (see block vertebra) DDx compression fracture
66	Clinical Data Two or more hemivertebrae on the same side are likely to result in scoliosis that progresses as the child grows. 2 hemivertebrae on opposite sides, scoliosis may be slight. Segmented hemivertebrae: - will progress more than nonsegmented hemivertebra Nonsegmented hemivertebrae: (block hemivertebrae) - these should not progress;
67	Imaging laterally wedged vertebra short segment scoliosis segmented and non segmented extra ribs other associated spinal anomalies
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69	Schmorls Nodes (p. 349)
70	Clinical Data nucleus pulposus herniates through vertebral end plates. embryological blood vessels osteoporosis trauma back pain? very common associated with degenerative disc disease?
71	Imaging well-defined defect involving the endplate giant Schmorl’s nodes disc space narrowing morphological vertebral body changes decreased signal on MRI associated with Scheurman’s disease
72	Imaging giant Schmorl’s nodes associated with degenerative disc disease vacuum phenomenon elongation of the vertebral bodies Scheurermann’s disease aka juvenile discogenic disease
73	Limbus Vertebra (p. 343)
74	Clinical Data herniation of nucleus pulposus through secondary growth centers the ring apophysis usually an isolated anomaly common in the lumbar spine Significance can be associated with Scheuermann’s disease / juvenile discogenic disease DDx fracture smooth corticated margins lack of clinical history vertebral body avulsion uncommon in the lumbar spine
75	Imaging free fragment at the anterior, superior body margins well corticated can be associated with juvenile discogenic disease
76	Nuclear Impression notochordal persistance (p. 349)
77	Clinical Data smooth concave defect at the posterior 1/3 the vertebral body notochordal persistance Significance no clinical significance. DDx fracture Schmorl’s nodes
78	Spina Bifida Occulta
79	Spina Bifida (p. 354) refers to a local failure of primordia of the two laminae to unite leaves vertebral canal open dorsally (spinal rachischisis, or spina bifida) spina bifida occulta defect involves primarily bone, but skin may be attached to dura, spinal cord, or nerve roots by fibrous bands Meningocele meninges may protrude Myelomeningocele spinal cord may protrude
80	Clinical Data small defect in closure of laminae most common at L5 and S1 may be seen at any level Significance no clinical significance should not be considered in radiographic pre-employment screening
81	Imaging defective fusion of the lamina at the midline knife clasp syndrome spina bifida at S1 with an enlarged of L5 spinous process Painful on extension???
82	Transitional Vertebra (p. 354) lumbarization sacralization
83	Clinical Data incomplete segmentation at transitional levels of the spine difficult associated with back pain association with disc herniation at the adjacent superior segment accessory joint degeneration may occur spinal segments demonstrate characteristics of: Sacralization L5 fuses to sacrum Lumbarization S1 becomes lumbar spine like (L6) segmentation has variability fusion accessory joint formation
84	Imaging spatulated, hyperplastic transverse process variable accessory joint formation occasional accessory joint degeneration hypoplastic disc accurate segment count must include T1
85	variations
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87	Intervertebral disc hypoplasia (p. 343) Common cause of narrowed disc space, especially common in young patients where degeneration is not likely
88	iliolumbar ligament calcification and transitional segmentation
89	Facet Tropism (p. 340)
90	Clinical and Imaging Data asymmetric presentation of the facets coronal and sagittal facets at one level commonly L5-S1 Significance clinical association variable no clear evidence of association with degenerative disc disease or back pain
91	Transverse Process Accessory Joint
92	Persistent Apophyses and Epiphyses
93	Clinical and Imaging Data extremely common do not confuse the fracture use the history learn where they “live” transverse processes spinous processes ring apophyses trochanters
94	Imaging
95	persistent apophysis of the ulna
96	os acetabuli
97	Oppenheimers Ossicles
98	Congenital absence of pedicles
99	Agenesis of the pedicles (p. 328)
100	Clinical Data anomalous formation of the neural arch creates enlargement of the opposite neural arch pedicle sclerosis DDX not to be confused with bone destruction/metastatic bone disease may require CT/MRI confirmation
101	Imaging absent pedicle opposite pedicles sclerosis no evidence of bone destruction Additional Studies CT obliques
102	confirmed metastatic bone disease
103	Hahns Groove Embryonic vascular channel No significance
104	Congenital Hip Dysplasia (p. 427)
105	Clinical Data displacement of the hip with acetabular dysplasia etiology related to hip joint laxity and inverted labrum girls more common left hip +ve Ortolanis/Barlows Significance must be a newborn diagnosis delayed diagnosis results in early osteoarthritis
106	Developmental Dysplasia of the hip
107	Developmental Dysplasia of the hip (p.) Clinical: Location of limbus may complicate conservative management MRI, ultrasound needed to determine if limbus is everted
108	Imaging Putti’s triad. Absent or small proximal femoral epiphysis Lateral displacement of femur Increased inclination of acetabular roof Additional Studies ultrasound arthrography CT
109	Specific roentgenometrics (p.197)
110	Acetabular Protrusion (p. 1074) Developmental Pathological Joint disease Bone Softening Pagets
111	Kohlers Line
112	Femoral herniation pits capsule/synovial indentations Normal? An HP of the femoral neck is considered to be the result of mechanical stress from the hip capsule and related musculature on the superolateral quadrant of the femoral. This region of the femoral neck is prone to developing a reaction area composed of fibrocartilaginous elements that may penetrate tiny defects in the degenerative cortex leading to the formation of an HP.
113	Pubic Synchondrosis variant of maturation point of fusion between the ischium and pubis Significance none DDX tumor fracture
114	Vascular Groove normal variant impression from vascular pulsation no significance
115	paraglenoid sulcus normal variant vascular groove female pelvis
116	Carpal Coalition (p. 384) fusion of carpal bones lunate to triquetrum most common may be associated with other congenital anomalies
117	Negative ulnar variance (p. 387) Relative shortness of ulna compared to radius, measured by comparing the distal ends of each bone. Associated with avascular necrosis
118	Nutrient canal (p. 387) At times, the nutrient artery appears as an oblique radiolucent defect of bone
119	Supracondylar Process exostosis at the anterior and distal humerus Struthers ligament at the distal aspect Significance may fracture compression of median nerve and vascular structures DDx osteochondroma
120	Bipartite Patella (p. 391)
121	Clinical Data incomplete unification of multiple ossification centers 80% bilateral fragment at the superior, lateral aspect smooth and well corticated may be subject to trauma
122	Bipartite Patella merchant view of the patella “patella points lateral”
123	growth arrest lines normal variant no clinical significance DDx stress fracture too well-defined lack of appropriate history
124	Accessory Ossicles of the Foot (p. 391) os trigonum os tibiale externum os supranaviculare os peroneum os intermetatarseum and a bunch more – look them up!
125	os trigonum
126	os tibiale externum
127	os intermetatarseum
128	os peroneum
129	Tarsal Coalition talocalcaneal synostosis loss of the subtalar joint best imaged on CT
130	Tarsal Coalition fibrous or osseous conjunction between tarsal bones talo-navicular talo-calcaneal talar beak associated Significance pain spastic flat foot Additional Studies CT/MR
131	Soft Tissue Calcification dystrophic tissue trauma inclusive of infection metabolic/metastatic widespread (metastatic) soft tissue calcification secondary to metabolic and endocrinological diseases physiological normal usually within cartilaginous tissue
132	Thyroid cartilage stylohyoideus ossification physiological anatomical variation Significance minimal clinical impact chiropractic precautions? Eagle syndrome neck pain (rare)
133	Imaging extends from the styloid process at the base of the skull to the hyoid bone may be segmented
134	Costal Cartilage Calcification
135	Costal Cartilage
136	Falx Cerebri Calcification calcification of the dura physiological no significance
137	Petroclinoid “Ligament” Calcification calcification of the dura physiological no significance
138	Pineal Gland Calcification physiological calcifications fifty percent of population should not exceed 10 mm pinealoma
139	Phleboliths calcified venous thrombi perirectal veins (not midline) normal dystrophic calcification
140	Lymph Node Calcification
141	Mesenteric Lymph Nodes granulomatous infection Tb Coccidio histoplasmosis not significant
142	Carotid Calcification
143	Diabetic Calcification
144	Vas Deferens Calcification diabetics dystrophic calcification no clinical significance associated vascular disease
145	Prostate Calcification