Motor Psychopathology
Catatonia
In catatonia, there is a disturbance of both mental state and psychomotor functioning. Often, Paper A concentrates on the motor function of catatonic patients, so it is that aspect of the condition which we’ll focus on. For purposes of understanding, the movement types demonstrated will be split into two categories: abnormal psychomotor activity and decreased psychomotor activity (modified from the ICD-11). The ICD-11 also has a third category, Increased Psychomotor Activity, which includes impulsivity and agitation.
Abnormal psychomotor activity
Echophenomena
This is an encompassing term for two conditions where the patient imitates the clinician (Ford, 1989)
- Echolalia – The patient repeats the speech.
- Echopraxia – The patient copies movements.
Grimacing
Spontaneous contraction of the facial muscles into odd facial expressions, which are not congruent with the situation. A grimace is often maintained for a prolonged period of time.
Schnauzkrampf is a variant of grimacing whereby the lips are pushed out and look like a snout (Casey and Kelly, 2019).
Mannerisms
Mannerisms are goal-oriented movements made by the patient that are often oddly exaggerated (Kaufmann et al., 2018). Movements seen include saluting.
Stereotypy
A patient makes repetitive movements; however, unlike mannerisms, they are not goal-oriented and are suppressible. These types of movements are also seen in autism spectrum disorder and intellectual disability.
Examples of movements seen are flapping of the hands and rocking of the body.
Posturing
This is where a patient spontaneously takes up a position against gravity and then holds this for a prolonged period of time (American Psychological Association, 2023). This is known as catalepsy when it is the examiner who places the patient in the held position.
Rigidity
There is increased muscular tone, leading to the resistance of movements.
Waxy flexibility
This is also known as cerea flexibilitas, and it is where the patient maintains any position in which their limbs are placed. There may be a little resistance to the movement by the patient.
Please note that the literature gives several different descriptions of catalepsy and waxy flexibility. I’ve adapted the ICD-11 definitions here for clarity.
Decreased psychomotor activity
Gegenhalten
This is also known as negativism. The patient refuses to obey commands or resists the movements of body parts, often using a force which is equal to that applied by the examiner (Wijemanne and Jankovic 2015). Negativism can lead to aversion, which is where the patient turns their body away from the clinician during an interaction.
Autonomic obedience
This is where a patient complies with all requests/commands with an exaggerated response (Wijemanne and Jankovic, 2015). They comply with these requests even if they would normally be regarded as dangerous. It is the opposite of negativism. The most famous (and memorable) demonstration of autonomic obedience was in the research done by Kraepelin (Casey and Kelly 2019), whereby he stuck a pin in the tongue of his patient every time his tongue was stuck out. The patient continued to stick out his tongue as requested despite the pain being inflicted on him.
Mitmachen and mitgehen (Rajagopal, 2007) are types of automatic obedience:
- Mitamachen – The patient can be put into any position by the examiner and does not resist this movement even if instructed to.
- Mitgehen – As with Mitmachen, the patient’s body can be placed in any position; however, this is a more extreme version whereby the limbs move much further than the force applied to them. In fact, it takes very little force to move a limb. This is also known as the ‘Anglepoise lamp’ sign (a phrase that crops up in exam questions).
Ambitendency
Here, the patient appears to be in conflict around moving their body. They will, therefore, make partially complete stilted movements that are goal directed (Casey and Kelly, 2019).
Stupor
A patient is alert. However, there is minimal interaction with the environment – Be that with no motor or verbal interaction (Wijemanne and Jankovic, 2015). This is seen in depressive states.
Extrapyramidal Side Effects
Extrapyramidal side effects (EPSEs) are probably the most common disorders of motor control that you will see in MRCPsych Paper A questions. We’ll discuss each one in turn, but I’ll provide a general overview here.
The four EPSE’s are:
- Akathisia.
- Dystonia.
- Parkinsonism.
- Tardive dyskinesia.
In the literature, EPSEs are often attributed to the dopaminergic antagonism of antipsychotics (especially first generation) at the D2 receptors. However, it is worth noting that studies have shown that those with a diagnosis of schizophrenia who are medication naive have higher rates of EPSEs than the general populous (Rybakowski et al., 2014).
In terms of medication culprits, first generation antipsychotics (such as haloperidol) carry the highest risk. Of the second-generation agents, risperidone carries the highest risk, whereas clozapine very rarely causes EPSEs (Divac et al., 2014). EPSEs usually occur within a short time of commencing an antipsychotic (hours to weeks), other than tardive dyskinesia, which has a much more delayed onset (often years).
Akathisia
This is the feeling described by patients as ‘inner restlessness’, which is manifested by the patient through the motor system, e.g. by pacing foot stamping (Salem et al., 2017). Akathisia normally occurs within hours and weeks of commencing an antipsychotic.
To manage this, a reduction in dose or switch to an alternative antipsychotic can be trialled. Propranolol is also used to have a good effect on managing restlessness. Akathisia, however, is often recognised as the most difficult EPSE to definitively manage.
Dystonia
A dystonia is a sustained muscle contraction, which is dose-dependent, that is especially seen with the use of IM haloperidol. This increases muscle tone, which leads to an abnormal posture. It often occurs within the first 2-5 days following administration of the offending drug (Pasricha et al., 2006). Young males are especially at risk.
Common forms include:
- Torticollis – The head turns to one side due to painful muscle spasms.
- Trismus – Commonly known as lockjaw.
- Opisthotonus – Arching of the back of the head and neck.
- Laryngeal dystonia – Notoriously difficult to diagnose but can be life threatening. Look out for stridor, shortness of breath and the patient grasping their throat.
- Oculogyric crisis – The eyes move in one direction, often upwards.
Management depends on the severity, but often, anticholinergic medication (such as procyclidine) is used; IM and IV forms act very rapidly and are used in emergency situations. Thought should be put into reducing the triggering anti-psychotic.
Parkinsonism
Symptoms of Parkinsonism include – Akinesia, resting pill-rolling tremor, rigidity (often described as ‘lead-pipe’ or ‘cogwheel’) and bradykinesia, which is the slowing of movements (Jankovic, 2008).
Akinesia
Akinesia is often thought of as a subset of bradykinesia, and it is the absence of movement. It is often seen in patients with Parkinsonism as a loss of facial emotion with exam questions using the phrase, ‘mask like expression’ or ‘serpentine’ stare.
Tardive dyskinesia
Tardive dyskinesia is a later onset EPSE in which the patient gets involuntary movements of their body, often of the face (oro-facio-bucco lingual movements), but it can also affect the trunk and body (Caroff, 2020). Movements often include repetitive lip smacking, tongue protrusion and grimacing.
Tardive dyskinesia can be very distressing for patients, not only due to the stigma associated but also due to its painful nature. Oro-facio-bucco lingual movements may lead to issues with eating, drinking, and even speaking. Patients with long term exposure to antipsychotics are especially susceptible to tardive dyskinesia.
Management is to consider reducing/changing/stopping the offending antipsychotic if possible. Clozapine is a good alternative. Tetrabenazine, a VMAT-2 inhibitor, is licensed as an add-on for the management of tardive dyskinesia but is yet to see widespread clinical use.
Tics & Tremors
Tics
Tics are repetitive, rhythmic movements which are spontaneous and seen more commonly in boys (Centers for Disease Control and Prevention, 2022). They can occur in motor and / or vocal modalities but can only be partially resisted by the individual (and so can be temporarily suppressed), though this is often difficult.
Tic disorders
As per the ICD-11:
- Tourette’s syndrome – Involves tics in BOTH the motor and verbal modalities, with multiple motor symptoms and at least one verbal symptom for diagnosis (with symptoms occurring for >12 months).
- Chronic tic disorder – These occur in EITHER the motor or verbal modalities, with symptoms lasting >12 months.
- Transient tic disorder – Symptoms lasting <12 months.
It is worth noting that tics can also be seen in infections (such as CJD) and triggered by medications (such as cocaine and other stimulants).
Tremors
These are rhythmic, involuntary movements of at least one body part. Tremors are the most common movement disorder that you’ll encounter in psychiatry and most commonly affect peripheral body parts such as the hands.
Extrapyramidal tremors
These are resting tremors, which are around 4Hz (Sanders and Gillig, 2012). These are seen in Parkinson’s disease, Parkinson’s plus, Parkinsonism and Lewy body dementia. The movement is often witnessed in the hands (pill rolling tremor) and limbs.
Cerebellar tremor
This is also known as an intention tremor and happens in the 4-6 Hz frequency. Evidence suggests that lesions in the dentate nucleus and superior cerebellar peduncle often lead to this kind of tremor (Thach et al., 1992).
Causes include alcoholism, multiple sclerosis, stroke and Friedreich’s ataxia.
Essential tremors
It is also known as benign essential tremor, which is seen on activity and around 4-12 Hz. The patient will often see symptoms symmetrically in the hands, head or even the voice (Louis, 2001). There is often a strong family history (Bain et al., 1994), and the patient may note that the tremor improves with alcohol. If the symptoms interfere with quality of life, then a beta blocker such as propranolol can be utilised (Pal, 2011).
Physiological tremor
A physiological tremor is a normal phenomenon. Due to it occurring in the 8-12 Hz frequency (Marshall, 1961), it cannot always be seen by the eye. It does, however, become noticeable in activity for some individuals under certain circumstances, including:
- Anxiety states.
- Medications – Salbutamol, lithium.
- Drugs – Caffeine, alcohol and opioid withdrawal.
- Medical conditions – Hypoglycaemia, hyperthyroidism, pheochromocytoma.
Physiological treatments, on the whole, do not need treatment. Propranolol, however, has been used to good effect for individuals who want to suppress a tremor due to anxiety in triggering situations (such as when making a presentation).
Functional tremors
These are also known as psychogenic tremors (Deuschl et al., 2004) and often have a sudden onset, usually associated with a stressful life event. The tremor is seen at rest and on activity and spontaneously remits.
Miscellaneous Motor Psychopathology
Athetosis
Slow, rhythmic, sinuous movements – Often described in exam questions as ‘worm like’ movements. It is often confined to the distal limbs and is seen in conditions such as cerebral palsy, stroke and Wilson’s disease.
Chorea
These are brief, irregular movements which are often described as ‘dance like’ in that they flow from one muscle to the next. Distinguishing chorea from athetosis can be difficult; however, in chorea, the individual movements can be identified (like still images from a film), whereas in athetosis, there are just continuously flowing movements (Sanger et al., 2011). There are many causes, including Huntington’s disease and infections.
Sydenham’s chorea
This is a syndrome seen in post-streptococcal infections, such as rheumatic fever (Gordon, 2008). It is most likely due to an immune reaction against the basal ganglia.
Hemiballismus
This is where there are involuntary, large flailing movements of the proximal limbs. Causes include stroke, infections and hyperglycaemia. Hemiballismus are thought to be due to damage to the subthalamic nucleus and other basal ganglia structures (Grandas, 2011).
Myoclonus
These are involuntary jerking movements due to the contraction of muscles (Kojovic et al., 2011). Myoclonus can be innocuous:
– Benign sleep myoclonus of infancy – Normally occurring phenomenon in the first 6 months of life, where they occur during sleep.
– Hypnic jerks – Also known as sleep starts, whereby the myoclonic jerks occur when falling asleep.
But it can also be due to other neurological conditions such as epilepsy and multiple sclerosis.
Gait Disorders
The following table is adapted from the paper ‘Gait and its Assessment in Psychiatry’ by Sanders and Gillig (2010) and describes the disorders in gait commonly encountered in psychiatry. I have simplified this table to indicate how the gait is commonly described for exam purposes.
| Gait | Description | Associations |
| Antalgic | In lay terms – A limp.
It presents as a shortened stance phase relative to the swing. |
Orthopaedic injury (acute or prolonged). |
| Ataxic | Wide based, irregular, unsteady gait.
Difficulty walking toe to heel (tandem gait). |
Cerebellar disease – Including strokes.
Alcohol related states – Acute intoxication; Wernicke’s. |
| Circumducted | It is seen in hemiparesis, whereby the leg is swung out and around. | Hemiparesis (e.g. secondary to stroke). |
| High-steppage | The leg is lifted higher than expected during the swing phase in order to prevent the foot from hitting the ground.
The foot appears floppy. Also known as neuropathic or equine gait |
Foot drop.
Multiple sclerosis. Guillain-Barre. |
| Magnetic | The feet appear stuck to the ground. | Normal pressure hydrocephalus. |
| Parkinsonian | Reduced arm swing, stooped posture, hesitation, large turning radius and festination (short shuffling steps). | Parkinson’s disease.
Parkinsonism (including drug induced). |
| Sensory Ataxia | Due to loss of proprioception, the foot will slam into the ground in order for the patient to be able to feel it.
Also known as ‘stomping gait’. |
Peripheral neuropathy.
Pernicious anaemia. Friedreich’s ataxia. Multiple sclerosis. |
| Spastic | Stiffness due to increased muscle tone almost presents as a kicking motion on the swing phase. | Demyelination (such as Multiple Sclerosis). |
| Scissoring | The knees and thighs cross over one another whilst walking due to increased tone of the hip adductors. | Cerebral palsy.
Multiple sclerosis. Spinal cord tumour or trauma. |
| Waddling | Also known as a myopathic gait.
It has a broad base. |
Weakness in the pelvic girdle.
Proximal myopathy. Congenital hip dysplasia. |
References
- World Health Organisation (WHO) (2019/2021) International Classification of Diseases, Eleventh Revision (ICD-11). Available online at: https://icd.who.int/browse11. [Accessed February 2023]
- Ford, R.A. (1989) ‘The psychopathology of echophenomena’. Psychological Medicine. 19(3):627-635.
- Casey, P. and Kelly, B. (eds) (2019) Fish’s clinical psychopathology: Signs and symptoms in psychiatry. Fourth edition. Cambridge: Cambridge University Press.
- Kaufmann C., Agalawatta N., and Malhi G.S. (2018) ‘Catatonia: Stereotypies, mannerisms and perseverations’. Australian & New Zealand Journal of Psychiatry. 52(4):391-393.
- American Psychological Association (2023). APA Dictionary of Psychology. Available online at: https://dictionary.apa.org [Accessed February 2023]
- Wijemanne S., and Jankovic J. (2015). ‘Movement disorders in catatonia’. Journal of Neurology, Neurosurgery & Psychiatry 86:825-832.
- Rajagopal, S. (2007) ‘Catatonia’. Advances in Psychiatric Treatment. Cambridge University Press, 13(1):51–59.
- Rybakowski J.K., Vansteelandt K., Remlinger-Molenda A., et al (2014). ‘Extrapyramidal symptoms during treatment of first schizophrenia episode: results from EUFEST’. European Neuropsychopharmacology. 24:1500–5
- Divac N., Prostran M., Jakovcevski I., and Cerovac N. ‘Second-generation antipsychotics and extrapyramidal adverse effects’. BioMed Research International 2014:656370.
- Salem H., Nagpal C., Pigott T., and Teixeira A.L. (2017). ‘Revisiting Antipsychotic-induced Akathisia: Current Issues and Prospective Challenges’. Current Neuropharmacology. 15(5):789-798.
- Pasricha P.J., Pehlivanov N., Sugumar A., and Jankovic J. (2006). ‘Drug Insight: from disturbed motility to disordered movement–a review of the clinical benefits and medicolegal risks of metoclopramide’. Nature Clinical Practice Gastroenterology Hepatology. 3(3):138-48
- Jankovic J. (2008). ‘Parkinson’s disease: clinical features and diagnosis’. Journal of Neurology, Neurosurgery & Psychiatry. 79:368-376.
- Caroff S.N. (2020). ‘Recent Advances in the Pharmacology of Tardive Dyskinesia’. Clinical Psychopharmacology and Neuroscience. 18(4):493-506.
- Centers for Disease Control and Prevention (2022). Diagnosing Tic Disorders. Available online at: https://www.cdc.gov/ncbddd/tourette/diagnosis.html [Accessed February 2023]
- Sanders R.D., and Gillig P.M. (2012). Extrapyramidal examinations in psychiatry. Innovations in Clinical Neuroscience. 9(7-8):10-16.
- Thach W.T., Goodkin H.P., and Keating J.G. (1992). ‘The cerebellum and the adaptive coordination of movement’. Annual Review of Neuroscience. 15:403–42.
- Louis, E.D. (2001). ‘Clinical practice. Essential tremor’. New England Journal of Medicine 345:887–891.
- Bain P.G., Findley L.J., Thompson P.D., et al. (1994). ‘A study of hereditary essential tremor’. Brain. 117:805–824.
- Pal P.K. (2011). ‘Guidelines for the management of essential tremor’. Annals of Indian Academy of Neurology. 14(1):S25-S28.
- Marshall, J. (1961). ‘The effect of aging upon physiological tremor’. Journal of Neurology, Neurosurgery and Psychiatry. 24(1):14- 17
- Deuschl, G., Köster, B., Lücking, C.H. and Scheidt, C. (1998). ‘Diagnostic and pathophysiological aspects of psychogenic tremors’. Movement Disorders. 13: 294-302.
- Sanger T.D., Chen D., Fehlings D.L., et al. (2010). ‘Definition and classification of hyperkinetic movements in childhood’. Movement Disorders. 25(11):1538-1549.
- Gordon, N. (2008). ‘Sydenham’s Chorea, and its complications affecting the nervous system’. Brain and Development. 31:11-14
- Grandas F. (2011). ‘Hemiballismus’. Handbook of Clinical Neurology. 100:249-60.
- Kojovic M., Cordivari C., and Bhatia K. (2011). ‘Myoclonic disorders: a practical approach for diagnosis and treatment’. Therapeutic Advances in Neurological Disorders. 4(1):47-62.
- Sanders R.D., and Gillig P.M. ‘Gait and its assessment in psychiatry’. Psychiatry. 7(7):38-43.
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