Chrissy Durrough Lugge
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Hi Liping,
I am going to revise this question a bit to be more clear. The question specifically pertains to the Behrman and Harkema article and treadmill training. Walking at faster speeds taps into our central pattern generators to facilitate a more normal and reflexive walking pattern.
For functional overground walking, bracing is necessary and effective for many individuals post-SCI. In the right circumstances and with adequate manual assistance, some of these patients may benefit from treadmill training without bracing.
Multiple nerve roots are responsible for many movements. You can view the table on this site to see the complexities: https://www.physio-pedia.com/Spinal_Cord_Muscle_Innervation
The ASIA exam and generally accepted myotome testing for UE screens have some minor differences, but they are both correct.
The key here is that the onset of his symptoms coincided with a severe bacterial infection. Some antibiotics are ototoxic and cause irreversible bilateral vestibular loss.
Individuals with profound hamstring and/or plantarflexor weakness may have knee hyperextension in mid-stance due to a lack of eccentric control of knee extension (i.e., normally functioning hamstrings or plantarflexors could prevent the knee from snapping into hyperextension).
In cupulolithiasis, the otoconia are attached to the cupula rather than free-floating in the canals. Cupulolithiasis is rarer are “stickier” than canalithiasis, but not necessarily more severe. Yes, same principal for anterior and posterior canal cupulolithiasis – convert to canalithiasis, then treat.
1. Habituation exercises are inappropriate for patients with bilateral vestibular loss, because they are designed to decrease unwanted responses to vestibular signals rather than to improve gaze or postural stability (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259492/). Adaptation exercises, on the other hand, may be beneficial if there is some residual vestibular function. Adaptation exercises aim to improve gaze stability while habituation exercises aim to desensitize someone to provocative motions.
2. In this study, the 7 of 8 subjects with bilateral vestibular hypofunction had improvements in their dynamic visual acuity and 5 of 8 returned to their age-referenced range for DVA. However, none of them had improvements in their VOR gain as measured by the rotary chair test. From this, we can conclude that adaptation exercises do not change the vestibular system itself and changes are likely due to central programming/neuroplastic changes.
The authors phrased it like this: “We do not think that this improvement in DVA reflected a change in vestibular function. We found no evidence of a change in VOR gain as measured by rotary chair testing…A second mechanism for improvement in DVA may be the use of central preprogramming of other types of eye movements to improve gaze stability.19-21 We have previously demonstrated that subjects with unilateral vestibular hypofunction have better visual acuity during self-generated head rotation than during unpredictable head movements.14 This suggests that central programming of eye movements may contribute to gaze stability during predictable head movements. Centrally programmed eye movements have been described in patients with peripheral vestibular hypofunction and include preprogrammed saccades that occur during the head movement as well as high-velocity, slow-phase eye movements (velocities of 80°/s to 120°/s)”
This is similar to stroke recovery. Following stroke, there are no changes to the core ischemic zone. Improvements happen because other areas of the central nervous system adapt to take over the lost function.
1 and 2. If a person has knee hyperextension ROM, they can use a KAFO with an offset knee joint and an unlocked knee to allow free motion into knee flexion during swing phase and during sit-to-stands. They will rely on their knee hyperextension for stance stability – the KAFO will not block hyperextension unless it has an additional stop installed. The patient will require adequate voluntary muscle control to hyperextend their knee during stance phase. The KAFO hinge would be aligned posterior to the patient’s knee joint. When the person hyperextends their knee, it moves the ground reaction force anterior to the knee, creating an extension moment.
Here’s another explanation from this article (https://www.sciencedirect.com/topics/nursing-and-health-professions/knee-ankle-foot-orthosis):
“An offset joint is a hinge placed posterior to the midline of the leg so that the patient’s weight line falls anterior to the joint. This stabilizes the knee during the early stance phase of gait when the wearer is on a level surface and does not hamper knee flexion during swing or sitting. The joint may, however, flex inadvertently when the wearer walks down a steep ramp. An offset joint should not be used by the patient with a knee flexion contracture because the contracture will make the floor reaction force pass posterior to the knee.”3. Someone may be hyperextending their knee/plantarflexing their ankle during stance phase as a compensation for quad/PF weakness to prevent uncontrolled tibial advancement during stance phase. A DF stop can control tibial advancement and may allow the person to avoid knee hyperextension.
Hi Claudia,
I haven’t seen the question to which you’re referring, but I will try to provide some information without that context.AFOs generally block ankle plantarflexion ROM to facilitate foot clearance during gait. Regardless of footplate length, I think it would be expected that AFOs will block PF ROM. I did find one article indicating that AFOs with full-length footplates produce increased stance phase PF moments compared to no AFOs (wherease 3/4 footplates were no different than no AFOs). That same study found that AFOs with 3/4 footplates resulted in significantly less than normal dorsiflexion in late stance. It was hypothesized that AFOs with full-length footplates increased DF ROM and PF moment in late stance by delaying or impeding heel rise more than the 3/4 footplate.
Here is a link to the article: https://www.archives-pmr.org/article/S0003-9993(09)00122-1/fulltext#:~:text=Both%20AFOs%20with%20full%2Dlength,foot%2Dplate%20resulted%20in%20ankle
Hi Alex,
In my experience, the BBQ roll is just for canalithiasis. For cupulolithiasis, we generally want to start with a fast movement like the modified Liberatory/Semont to displace the otoconia and convert cupulolithiasis to canalithiasis. After conversion, we would then do a canalithiasis treatment like the BBQ roll.Great question! Stages 1.5 and 2.5 were added to the original H&Y scale as refinements – and there are only subtle differences between stages 2 and 2.5 (and 1 and 1.5).
Basically, if someone has bilateral symptoms and is starting to demonstrate some changes to balance but is not yet losing their balance, they are considered stage 2.5. This can be quantified with the retro pull test where maintaining balance in 3 or more steps would be considered stage 2.5 (whereas 1-2 steps is stage 2).
The best explanation is from the American Parkinson Disease Association (https://www.apdaparkinson.org/article/stages-in-parkinsons/):
“In the original H-Y system there were no stages 1.5 and 2.5. These were added later as refinements. In stage 1.5, only one side is affected, but one can see symmetric problems on both sides such as reduced facial expression on both sides, stooped posture on both sides, or reduced arm swing on both sides. In stage 2.5 both sides are involved plus there is a mild impairment of balance, but not loss of balance. To test for this, the patient is told that he will be pulled backward and to take a step back to try to prevent a fall. The patient is then pulled backward firmly. It is considered normal to take one or two steps, but if three or more are taken and balance is recovered, it is considered stage 2.5 (or 1.5 if there are no signs of PD on the better side).”Hi Claudia,
The NCS exam will be curved. After the exam window closes, a careful analysis of all exam questions will be completed. Here are some details provided by the ABPTS:
“What happens between my test completion and notification?
Although there is a time lapse between the close of the examination window and the availability of examination results, there is a lot activity occurring during this period of time. Key validation takes place after the exam window closes in March. Key validation is a process of preliminary scoring and item analysis of the exam data, followed by careful evaluation of the item-level data, to identify potentially flawed or incorrect items prior to final scoring. During April and early May, standard setting committees are convened at PSI to participate in content-based standard setting studies. The outcome of each committee’s standard setting meeting is the recommendation of a passing standard of each of the specialty examinations during their May meeting. PSI then scores the specialist certification examinations and candidates are notified of their exam results as soon as this information is received by the specialist certification office.”https://specialization.apta.org/become-a-specialist/exam-specialty-resources/exam-day
Hi Erin!
The vestibulo-ocular reflex is the reflex that allows us to maintain gaze stability while turning our heads (our eyes move equal and opposite to our head). VOR cancellation is a central vestibular function that allows us to override that reflex in instances when we want our eyes and head to move together.VOR is tested with the head impulse test and/or by measuring dynamic visual acuity.
VOR cancellation is screened by sitting in front of a patient, turning their head side-to-side, and asking them to keep their eyes focused on your nose. You will move side-to-side with the patient, forcing them to suppress their VOR. It might be easier to see someone performing the screen: https://www.youtube.com/watch?v=7Nw3TgieAjI
Hi! The cut-off changed just in the past few years. The article that showed 50/56 to be the cut-off was published in 2017, but I feel like it has only recently been the generally accepted value. 50/56 is cited in the ANPT’s Core Outcome Measures CPG, so I think it is fair game on this year’s exam.
Here’s a link to the Core Outcome Measures CPG: https://www.neuropt.org/practice-resources/anpt-clinical-practice-guidelines/core-outcome-measures-cpg
And the BBS pocket guide that includes score interpretation and references: https://www.neuropt.org/docs/default-source/cpgs/core-outcome-measures/berg-balance-scale-pocket-guide-proof-8.pdf?sfvrsn=8fe25043_0
Hi Alyson,
You are correct that the vestibular hypofunction CPG is related to peripheral vestibular dysfunction. Here is a great recent article discussing vestibular rehab for central vestibular dysfunction: https://www.tandfonline.com/doi/full/10.1080/14737175.2022.2106129This is part of the authors’ commentary on cerebellar strokes:
“Rehabilitation during the acute phase of cerebral infarction can effectively improve the quality of life. Therefore it is crucial that appropriate rehabilitation strategy should be used for patients with cerebellar infarction in the acute phase [154,155]. Some scholars found that balance exercises can improve the motor coordination by remodeling nerve synapses and activating astrocytes to improve the patient’s balance. However, early post-stroke multisensorial training, under visual deprivation with somatosensorial and vestibular stimulation, could be more effective than a traditional approach based on neurodevelopmental concepts [156,157]”These authors recommend VOR suppression/cancellation exercises, VOR memory/imaginary targets, anti-saccades, and memory saccades (all described in the article). Additionally, I have found postural control training, gait training, and VOR exercises to be important and effective in managing central vestibular dysfunction.
The prognosis for central vestibular dysfunction tends to be poorer than for peripheral disorders, with slower and less complete recoveries.
Chrissy
1) This question was written when the falls risk cut-off for the BBS was 45/56. It has been updated to have one correct answer.
2) You’re correct that both decreased foot clearance and increased force at initial contact can result from impaired sensation. This patient has an acute/sub-acute CVA as he has just been admitted to inpatient rehab. At this point, it is more likely that we will see decreased foot clearance during swing phase due to the inability to feel where his feet are in space and to increase sensory input through the floor. As the patient progresses and can consistently clear his feet and achieve heel strike at initial contact, we might see foot slap during loading response.
3) Figure 1 in the Fritz and Lusardi paper shows how walking speed is linked to discharge location. Walking speeds <0.1 m/s indicate increased likelihood of being discharged to a SNF while walking speeds >0.1 m/s indicate a discharge to home is more likely.
4) This patient was referred for back pain but presents with concerning signs of neurologic dysfunction. Given that a source of these signs has not been identified, the therapist’s best recommendation is for the patient to receive immediate medical attention. Because the patient’s symptoms have been gradually worsening, spinal neoplasm is more likely than Guillain-Barre syndrome. This patient has a number of red flags warranting immediate medical attention (age >50, symptoms radiating below the knee, atypical pain that is not affected by position changes, incontinence).
Here is the abstract from an article about red flags in acute low back pain (https://www.consultant360.com/peer-reviewed/acute-low-back-pain-recognizing-red-flags-workup#:~:text=%E2%80%9CRed%20flags%E2%80%9D%20include%20pain%20that,of%20a%20severe%20or%20rapidly):
A focused history and physical examination directed towards uncovering signs that suggest a serious underlying cause of low back pain are crucial. “Red flags” include pain that lasts more than 6 weeks; pain in persons younger than 18 years or older than 50 years; pain that radiates below the knee; a history of major trauma; constitutional symptoms; atypical pain (eg, that which occurs at night or that is unrelenting); the presence of a severe or rapidly progressive neurologic deficit; urinary and/or fecal incontinence; poor rectal tone; and a history of malignancy. These markers provide a cost-effective means of guiding your selection of laboratory and diagnostic imaging studies.
